Term
|
Definition
*fibroblasts proliferate in the wound and secrete glycoprotein and collagen
*epidermal cells migrate from the wound edge
*granulation tissue is formed from macrophages, fibroblasts and new capillaries |
|
|
Term
|
Definition
*fibroblasts secrete collagen to strengthen the wound
*occurs to reorganize fibers along tension lines
*contracts increasing tissue integrity
*epidermal cells grow over connective tissue to close the wound
*cells that are no longer needed are removed by apoptosis |
|
|
Term
|
Definition
makes a scaffold, macrophages inside, , these produce cytokines these can cause : platelet aggregation and degranulation, blood clotting, hemostasis, immigration of cells, removal cell debris, secrete growth factors
*leads eventually to wound closure and extracellular tissue remodeling |
|
|
Term
|
Definition
includes proteoglycans, fibrin, platelets
*It refers to the process of keeping blood within a damaged blood vessel |
|
|
Term
|
Definition
(1) Haemostasis
(2) Inflammation
(3) Proliferation
(4) Remodling |
|
|
Term
| cells contributing cytokines to healing |
|
Definition
| epithelial cells (keratinocytes on top of the skin), endothelial cells (grab neutrophils to help clean up), platelets, neutrophils, lymphocytes, macrophages, fibroblasts |
|
|
Term
|
Definition
colony stimulating factor
-produces more macrophages
-from level of the bone marrow makes produce more stem cells to help in healing |
|
|
Term
|
Definition
| term for the non-collagenous components of extracellular matrix. Cells are surrounded by extracellular matrix in tissues, which acts as a support for the cells. Ground substance traditionally does not include collagen but does include all the other proteinaceous components, including proteoglycans, matrix proteins and water. The non-collagenous components of extracellular matrix will vary depending on the tissue where it is found. |
|
|
Term
| Proliferation (Fibroplasia) |
|
Definition
*occurs 2-3 days after the wound
*starts even before inflammatory phase has ended
*fibroblasts enter wound site, begin to proliferate
*fibroblasts lay down ground substance and TYPE III collagen (scaffold for cell migration)
*PDGF (platelet derived growth factor), TGF, and fibronectin encourage proliferation and migration |
|
|
Term
| Proliferation : Granulation tissue |
|
Definition
| includes: new blood vessels (leaky so edema), fibroblasts, inflammatory cells, endothelial cells, myofibroblasts, provisional extracellular matrix (fibronectin, collage, glycosaminoglycans, proteoglycans) |
|
|
Term
| Proliferation : Collagen deposition |
|
Definition
| collagen produced by fibroblasts (type III), secretion 2-3 days after, peaks 2-3 weeks, increases wound strength, scaffolding for inflammatory, endothelial, and connective tissue, at the end cells apoptose, wound is collagenounous and less cellular. |
|
|
Term
| Proliferation : Epithelialization |
|
Definition
*epithelial cells migrate across granulation tissue and collgen matrix
* if bm is intact epithelial cells replaces w/in 3 days
* if bm disrupted then re-epithelialization has to occur from wound margins |
|
|
Term
|
Definition
outsides and down toward the center
*if wound is big it can start in the middle |
|
|
Term
| Proliferation : contraction |
|
Definition
*begins one week after injury
*fibroblasts differentiate into myofibroblasts
*wound contracts to reduce size of wound (40-80%) around the 'axis of contraction' |
|
|
Term
|
Definition
*at this stage collagen production = degradation
*lasts 1 year (approx)
*Type III degraded, Type I replaces (stronger type)
*Type I rearranged, cross-linked, and aligned along tension lines to increase tensile strenghts |
|
|
Term
| Factors the retard wound healing |
|
Definition
Local Factors : blood supply, mechanical stress, foreign body, necrotic tissue, etc..
Systemic factors = age, anemia, malnutrition, obesity, Vitamin deficiency |
|
|
Term
|
Definition
*deficient scar formation leading to reopening of a previously closed wound.
*is an example of dysregulated wound healing
*Risk factors : age, diabetes, obesity, scurvy (vit C) |
|
|
Term
|
Definition
Specialty type of scar that results from overgrowth of repair tissue (shiny fibrous node)
*not a hypertrophc scar, mostly collagen type III then replaced by type I
-common in young females, earlobes, sternum, shoulders, upper back
-treatment with surgery, compression, steroids, cyro, lasers |
|
|
Term
|
Definition
| when contraction occurs too long or too an extreme, caused deformities (myofibroblasts) |
|
|
Term
|
Definition
*mineralization of soft tissue w/o a systemic mineral imbalance
*reaction to a chroic inflammation
*Hydroxyapatite crystals deposit in previously damaged tissue
*examples : tb, fat necrosis (pancreatitis), infarcts, thrombi, hematomas, dead parasites
*lymphocytes and macrophages try to get rid of but cannot! |
|
|
Term
| How do neutrophils, lymphocytes, and monocytes get activated? |
|
Definition
|
|
Term
|
Definition
| *small secreted proteins, produced de-novo (on the spot, have to act quickly), specific in binding and response, involved in signaling, inflammation and hematopoiesis, act over short distances, short half-life, effective at LOW concentrations, there is tight control over their concentrations and actions |
|
|
Term
|
Definition
*bind to specific receptors, binding is through second messenger systems (Tyrosine kinases, alters cell behavior ;gene expression', synergistically acting or antagonistically)
*direct development, maturation, localization, interactions, activation and lifespan
*Essential role in innate and adaptive immunity |
|
|
Term
|
Definition
| *increasing or decreasing expression of membrane proteins, cellular proliferation, secretion or effector molecules that alter cell function |
|
|
Term
|
Definition
Autocrine = act on cell that ssecreted it
Paracrine = act on nearby cells
Endocrine = act on distant cells
*can be more than one type (pleiotropy)
*actions are redundant (several cytokines can elicit same response)
*synergistic or antagonisitic |
|
|
Term
| Cells that make cytokines |
|
Definition
*Mostly Macrophages and innate immune cells
*Helper T lymphocytes
*Th1 = stimulate cellular immunity and inflammation
Th2 = stimulate B cells to produce antibody (humoral immunity)
*Infected cells also make these |
|
|
Term
| Early cytokine response by innate immune cells |
|
Definition
IL-1,2,6,8,12, TNF-alpha
*produced by macrophages |
|
|
Term
| Cytokines and innate immunity |
|
Definition
*Innate immune cells = macs, granulocytes, NK, B cells
*recognize and bind many antigens (PAMPs) with their Toll-like receptors (TLR or PRR) |
|
|
Term
|
Definition
| mannose, LPS< baceria flagellin, lipoeichoic acid from gram pos bacteria, peptidoglycan, nucleic acid variants from viruses (unmethylated)etc... |
|
|
Term
|
Definition
*activates the production of cytokines
*IL-12 = stimulates production Th1 cells
*IL-^ = suppresses regulatory T cells (double negative) |
|
|
Term
|
Definition
1) resolve infection
2) stimulate adaptive immunity |
|
|
Term
|
Definition
*infected cells can signal their own destruction with INF (interferons), before infection spreads to other cells
*are made and released by lymphocytes in response to pathogens. |
|
|
Term
| Helper T cells as liaison btw innate and adaptive immunity |
|
Definition
*Helper T cells are the "middlemen" of the adaptive immune system. Once activated, they divide rapidly and secrete small proteins called cytokines
*There are helper 1 T cells (produce interferon-gamma which activates macrophages to kill bacteria and induces B cells to make opsonizing antibodies to help with cell mediated immunity
*most die after the infection is resolved, some remain as memory cells |
|
|
Term
| Cytokines and adaptive immunity |
|
Definition
| *middlemen, no phagocytic or cytotoxic ability, bind APCs, pass info to adaptive immune system, activate cytotoxic T cells, |
|
|
Term
| Helper T lymphocytes (Th1 cells) |
|
Definition
*produce IL-2, IFN-gamma, TNF-beta, to activate cytotoxic T cells and macrophages
*produce IL-3, GM-CSF to stimulate bone marrow to produce more leukocytes |
|
|
Term
| Helper T lymphocytes (Th2 cells) |
|
Definition
| *secrete IL-4,5,6,10 to stimulate antibody production by B cells |
|
|
Term
| Helper T lymphocytes (Th0 cells) |
|
Definition
*produce IL-2, 4, IFN gamma
-then differentiate into...
-Th1 (if IL-12 present, up-regulate CMI)
-Th2 (if IL-4 present, up-regulate humoral immunity) |
|
|
Term
|
Definition
*Specific names...
-lymphokine (from lymphocytes), monokine, chemokine, interleukin (one leuko that acts on another leuko)
*Common = Interferons, CSF/GFs, TNF (tumor necrosis factor), chemokines |
|
|
Term
|
Definition
*These stimulate immune cell proliferation and differentiation
-IL-1 (activate T cells), IL-2 (proliferation antigen-activated T and B cells, IL-4,5,6 (proliferation and differentiation of B cells), INF-gamma (macrophages), IL-3,7, GM-CSF (hematopiesis) |
|
|
Term
|
Definition
*produced early in infection
*interfere with viral replication and induce antiviral resistance in uninfected cells
*are alpha and beta : produced by cells infected with virus
*Gammma : released by Th1 and NK cells |
|
|
Term
|
Definition
*large group of cytokines
*mainly produced by helper T cells, or others like monocytes/macr., endothelial cells)
*many cause other cells to divide and differentiate. |
|
|
Term
|
Definition
*produced by monocytes/macro, dendritic cells, B cells
*Th cells (costimulation), B cells (maturation and proliferation), NK (activation)
*cause inflammation, acute phase resp, fever |
|
|
Term
|
Definition
*produced by Th1 lymphs
*growth, proliferation, activation activated T,B, NK cells
*stim of low affinity IL-2 receptor leads to induction of IL-2 and IL-2R-alpha chain for high T cell proliferation |
|
|
Term
|
Definition
*produced by helper t and NK cells
*for stem cell growth and differentiation
*for Mast cell growth and histamine release. |
|
|
Term
|
Definition
*produced by Th2 lymphocytes
*for B cell proliferation, differentiation, production Abs (IgG, IgE), antigen presentation (MHC I on macrophages)
*proliferation of T cells |
|
|
Term
|
Definition
*produced by Th2, mast, eosinophils cells
*for proliferation and differentiation of activated B cells, eosiniophil activation (allergies, asthma) |
|
|
Term
|
Definition
*produced by monocytes/macrophages, Th2 cells, stromal cells
*differentition of B cells into Ab-secreting plasma cells, differentiation of stem cells, acute phase response |
|
|
Term
|
Definition
*produced by bone marrow stroma, thymus stroma
*for differntiation of stem cells into progenitor B and T cells
*therefire is upregulating to produce more white cells |
|
|
Term
|
Definition
*produced by macrophages, endothelial cells
*for chemotaxis of neutrophils
*therefore draw early inflammatory cells to area of injury |
|
|
Term
|
Definition
*produced by Th2 cells
*for cytokine production by macrophages, activation of B cells |
|
|
Term
| Il-4,5,6, 10 involved in... |
|
Definition
*activation of B cells
*for humoral immunity |
|
|
Term
|
Definition
*produced by macrophages and B cells
*for differentiation of T cells into Tc cells, and NK activation
*especially for innnate immunity to further upregulate innate immune cells |
|
|
Term
|
Definition
*colony stimulating factor
*mostly for directing the division and differentiation of bone marrrow stem cells and precursors of blood leukocytes
*G (granulocyte), M (macrophage), GM (granulocyte) |
|
|
Term
|
Definition
*family of small cytokines secreted
*induced direct chemotaxis to guide migration
*other involved in homeostasis, angiogenesis, wound helaing
*GPCR receptors
*CHEMOtactic cytoKINES |
|
|
Term
|
Definition
*tumor necrosis factors
*produced by macrophages, mast cells, NK cells (TNF-alpha) , Th1, cytotoxic T cells (TNF-beta)
*trigger : acute phase rxn, cytokine exression, NO productions, phagocytosis by macs, apoptosis tumor cells |
|
|
Term
|
Definition
*transforming growth factors
*polypeptide growth factors
*produced by t cells, macs, others
*for chemotaxis and pdtion Il-1 by mon.macs
*syn. of IgA by plasma cells |
|
|
Term
| Control of leukocyte movement |
|
Definition
*injury causes inflammation, histamine release, mast and basophils
*increased permeability of vessels
*expression selectins, integrins (bind WBC surface)
*causes cell migration, rolling, extravasation |
|
|
Term
|
Definition
*large mononuclear cell, activated by TNF and other early cytokines
*function : APC (present Ag on MHC class II), prof phagocytes (Fc receptors), Produce cytokines (Il-1,6,7,12,15,18,TNF,CSF)
*can be further activated for adaptive immunity |
|
|
Term
|
Definition
*massive gram neg bacterial infection there is a large release of LPS
*hyperresponse causes high fever, multiple organ failure,etc...
*if pt survives succumb to secondary infection b/c immune from hyper to hypo0responsiveness
*causes= H1N1, avian flu, ARDS, smallpox |
|
|
Term
|
Definition
| *upregulate some kind of problem (infection) in the body |
|
|
Term
|
Definition
*causes nonspecific activation of T cells
*can be caused by viruses, bacteria |
|
|
Term
|
Definition
*short for antibody generator
*prompt immune response, usually proteins |
|
|
Term
|
Definition
*eat cells (self and non-self)
*break them up into bite-sized pieces, then take proteins or AA to present to helper T cells. |
|
|
Term
|
Definition
| *tolerated by the immune system (or if not causes autoimmunity) |
|
|
Term
|
Definition
| *contiguous surface of stratified squamous epithelium which flakes off, higher salt concentration from sweat gland as antiseptic, lower tempereature, sebaceous glands (acidic sebum), commensal bacteria, APC which sample environment and present pathogens. |
|
|
Term
| Natural barriers to infection besides skin |
|
Definition
| *tears (lysozyme), sailivary amylase, acidic pH of stomach, peristalsis, sneezing/coughing, cervical mucus and low pH, protatic fluid, hypertonic urine, silia of intestines |
|
|
Term
| When natural barriers fail (innate) |
|
Definition
*primitive form, immeadiate defense, PAMP, no long-lasting protection
*cells : NK, Mast, basophils and eosinophils, phagocytes, APCs |
|
|
Term
| When natural barriers fail (adaptive) |
|
Definition
*specialized, has memory, mounts stronger attacks each time pathogen is encountered
*cells : Helper T cells, cytotoxic T cells, B cells, memory cells |
|
|
Term
| Cells of Innate Immune System |
|
Definition
*WBC aka leukocytes
-NK = poke holes in pathigen
-Mast = degranulate, cause vasodilation
-Eosinophils & Basophils = allergy, parasitic infections
-Macs = phagocytes, APCs
-Neutrophils = phagocytes
-Dendritic = APCs |
|
|
Term
|
Definition
*presents antigens to helper T cells
*APC phagocytoses antigens, then breaks into smaller pieces, then displays them on cell surface (flag), presents to helper T cells
*TCR on T cell binds APC receptor that has antigen on it, this activiates the T cell and adaptive immunity |
|
|
Term
Dendritic cells
-where found
-what is purpose |
|
Definition
-found : skin, nose, lungs, GI tract
-MOST efficient APCs! |
|
|
Term
| B cells (in terms of as an APC) |
|
Definition
*can present antigen to which their Ab is directed
*INEFFICIENT APCs for most other antigens |
|
|
Term
| Interaction of APCs, T cells, and B cells |
|
Definition
*APCs phagocytose pathogen, APC migrates through lymph vessels to nodes, T cell recognizes antigen and becomes activated
*They mature during the trip (dont eat more pahtogens) |
|
|
Term
|
Definition
*innate immunity (primitive), round that look like lymphocytes with more cytoplasm
*recognize common antigens on surfaace of bacteria and foreign cells w/o prior exposure, kill infected and tumor cells
*use PERFORIN and GRANZYME to lyse |
|
|
Term
| Granulocytes (Neuts, Eos, Basos) |
|
Definition
*round, bigger tahn RBCs, multi-lobed nucleus, cytoplasmic granules, dont multiply in tissues (end cells)
*Neutro = acute inflammation, phagocytosis, chemtaxis
*Eos = allergy, parasitic
*Baso = inflammation, allergy |
|
|
Term
|
Definition
*Larger than neutrophils kidney-bean shaped nucleus, abundant cytoplasm with ground glass apperance
*circulate as moncytes, MACs in TISSUES
*macs not 'end cells'
*activated IFN secreted by lymphocytes, acute and chronic inflammation, APCs, prof. killers, better respiratory burst that neutrophils |
|
|
Term
|
Definition
*origin of immune cells (primary organ)
*in hollow int. of bones, 1/2 hematopoietic tissue and 1/2 fat, produces RBS, WBCs, platelets |
|
|
Term
| cells made in bone marrow that circulate |
|
Definition
*Granulocytes, until needed in inflammation, migrate to tissues
*Monocytes, become macs in tissues
*B lymphocytes in blood and lymphatic system, or reside in secondary lymphiod tissue until activated
*T lymphocytes are schooled in thymus |
|
|
Term
|
Definition
*cell mediated Immunity
*adaptive that involves activation of special lymphocytes (cytotoxic T, or CD8 T cells, that can recognize, bind, and kill
*Important: viral infections, transplant rejections
*Cytotoxic T cells activated by APCs, which activate helper (CD4) T cells, which activate CD8 cells |
|
|
Term
|
Definition
*distinguished from other B cells or NK cless b/c have T cell receptor (TCR) on cell surface
*btw the adaptive and innate |
|
|
Term
|
Definition
*express CD4 protein on cell surface
*act as interface innate and adaptive
*help activate adaptive response |
|
|
Term
|
Definition
*express CD8 protein on cell surface
*represent the CMI arm of adaptive
*target viruses and tumor cells |
|
|
Term
|
Definition
*remember specific Ags for many months-years (basis of immmunization)
*after infection a few of these are left so body can respond much quicker the next time |
|
|
Term
| Regulatory T cells (Tregs) |
|
Definition
*shut down CMI towards end of immune rxn
*suppress autoreactive T cells
*end of the immune response |
|
|
Term
|
Definition
*aka humoral immunity
*Abs produced by b cells and ciruclate in the blood
*APCs process antigen into bite-sized pieces, give to helper T cells, these activate B cells to become plasma cells to produce a specific antibody vs the pathogen |
|
|
Term
|
Definition
*second arm of the adaptive immune system
*play imp role in humoral immunity
*make Abs, serve as APC, persist as memory cells |
|
|
Term
| Active vs Passive Immunity |
|
Definition
*Natural Active = infection causes CMI or Ab-mediated immunity and memory vs future infections
*Artificial Active = vaccination
*Passive = transfer Abs through placenta or breast milk, adminstration of Abs (rabies, tetanus) |
|
|
Term
|
Definition
*use Toll-like receptors to recognize PAMPs (antigens)
*TLR activation stimulates these innate cells, and upregulated adaptive immunity
*Neutrophils, Macs, Dendritic cells can deal with about anything that comes along (many different types of TLRs) |
|
|
Term
|
Definition
*pathogen-associated molecular pattern
*molecules that are unique to microbes are recognized by innate immune cells as being foreign
*TLRs bind PAMPS, phagocytose the pathogen and upregulate adaptive immunity |
|
|
Term
|
Definition
*bacterial lipopolysacc. from Gram-bact.
*Flagellin
*Lipoteichoic acid from gram + bact.
*peptidoglycan
*dsRNA
*unmethylated CpG |
|
|
Term
|
Definition
*class of proteins on surface receptors that recognize PAMPs on innate immune cells
*recognize molecules that are shared by pathogens but not present on host
*homodimers (TLR1,6 -hetero)
*each one is SPECIFIC for certain microbe |
|
|
Term
|
Definition
*lipoteicoic acid on gram pos bacteria
*major component of cell wall G+ bacteria |
|
|
Term
|
Definition
|
|
Term
|
Definition
| *lipopolysaccharide on gram pos bacteria |
|
|
Term
|
Definition
| *Flagellin on motile bacteria |
|
|
Term
|
Definition
| *ssRNA, small synthetic compounds |
|
|
Term
|
Definition
| *unmethylated CpG on bacteria |
|
|
Term
|
Definition
| *prolifin on Toxoplasma, may recognize UTI bacteria |
|
|
Term
|
Definition
*pathogen may be phagocytosed
*antigens from pathogens may be presented to adaptive immune system
*stimulated innate immune cells may secrete cytokines to upreg. adaptive immunity
*viral = interferons may be released to reduced viral replication
*specific TLR will target specific components of adaptive immunity |
|
|
Term
| Receptors that are specific for one particular antigen |
|
Definition
*both B and T cells have surface receptors for antigen
*each cell has thousands of receptors
*all receptors are identical |
|
|
Term
|
Definition
*B cell receptors
*enable cell to bind to and be activated by and respond to a soluble antigen
*immature B cells made in bone marrow, migrate to spleen (transitional)
*a naive B cell has several different BCRs that may be similar to an antigen it encounters
*if loosely bind the gene rearrangement (somatic hypermutation)each successive generation better fit to antigen then will become a mature plasma cell
*if better fit then B cells survives and produces Abs |
|
|
Term
|
Definition
*is an antibody
*it a glycoprotein
*2 subunits, each containing heavy and light chain
*Y-shapre, top prongs contain variable regions that undergo mutation
*bottom prong is B cell binding site and is the constant region |
|
|
Term
| Light Chains and haavy chains of Ab |
|
Definition
Light chain : kappa, lambdaa
Heavy chain : M (IgM),gamma (IgG), alpha, delta , epsilion
*immature b cells have IgM or IgD heavy chains (switch depending on infection)
*no 2 b cells (except clones) same variable regions
*Abs become soluble once mutation of variable region is complete, and B cell becomes mature |
|
|
Term
| Genes involved in BCR heavy chains |
|
Definition
*51 VH(variable) gene segments
*27 DH(diversity) gene segments
*6 JH (joining) gene segments
* 9 CH
*V,D,J in heavy chains picked in bone marrow, mutated in periphery |
|
|
Term
| V(D)J rearrangement and joining |
|
Definition
*light chains = V and J regions
*heavy chains = V,D,J regions
*during b cell maturation each cell chooses 1v,1d,1j using RAG which cuts through DNA and splices them together, then somatic hypermutation (point mutation)
*THEREFORE not an antigen out there that the body cannot make an antibody against. |
|
|
Term
| Genes involved in BCR light chains |
|
Definition
*light chains = either kappa or lambda
*then V and J regions rearrange, mutate
in the secondary lymphoid organs |
|
|
Term
| Once variable regions are completed |
|
Definition
| *constant region changes to type of constant region needed for immmune response |
|
|
Term
|
Definition
*T cell receptors for antigens
*llok like BCRs
*variable (antigen binding site) and constant region
*2 chains, alpha(light, V and J) and beta (heavy, V,D and J) in 95% T cell
*5% have delta-gamma
*TOTALLY mature in thymus (unlike BCRs) |
|
|
Term
VDJ picked in the...
-differnce btw b and t cells |
|
Definition
*bone marrow
-maturation b cells in secondary lymphoid organ
-maturation t cells in the thymus |
|
|
Term
|
Definition
*cell engulfs some of the extracellular fluid including the material dissolved or suspended in it.
*part plasma membrane is invaginated and pinched off forming a endosome
*performed by all nucleated cells to engulf polar molecule that can pass through membrane
*nutrient uptake, receptor signalling, pathogen entry, NTs, receptor downregulation, antigen presentation, cell polarity, mitosis, growth and differentiation |
|
|
Term
| Clathrin-mediated endocytosis (micropincytosis) |
|
Definition
| *small vesicles containing protein, vesicles form clathrin-coated pits with receptors for endocytosis of LDL, transferrin, growth factors, Abs, |
|
|
Term
| Caveolae (micropinocytosis) |
|
Definition
*very small pits in membrane with no clatharin, in muscle, lung, fat, endothelium, fibroblasts
*used for uptake extracellular molecules, using receptors
*happens continuously |
|
|
Term
|
Definition
| *ruffle/invagination of cell membrane w/ large volume of ECF; fuses with lysosome for digestion |
|
|
Term
|
Definition
| *where specialized cell binds and englufs larger solid particles (dust, debris, microorganisms, apoptotic bodies) |
|
|
Term
| Clathrin-mediated endocytosis |
|
Definition
*how nearly all cells internalize nutrient, antigens, growth
*on almost every nucleated cell |
|
|
Term
| Some professional phagocytes |
|
Definition
*have Toll-like receptors on surface that recognize PAMPs, bind, and phagocytose
*neutrophils, monocytes, macs, dendritic cells, Mast cells
*so some extent baso and eos |
|
|
Term
|
Definition
*like basophiles, in tussues
*have granules (histamine, heparin, serotonin)
*degranulate when allergy, anaphylaxis and acute , cause vasodilation and chemotaxis |
|
|
Term
| Nonprofessional phagocytes |
|
Definition
*can be induced to become phagocytic under certain circumstances (intense inflammation)
*fibroblasts, epithelial, endothelial, mesenchymal, immature cells |
|
|
Term
|
Definition
*long spindle-shaped
*critical for wound healing
*produce ground substance (glycosaminoglycans) and fibers (reticular, collagen, elastin)
*mostly at END of inflammation during wound healing |
|
|
Term
|
Definition
*fried egg apperance (thin cytoplasm, round nucleus)
*line vessels and keep cells and plasma cells inside
*when disrupted enderlying collagen exposed, to initiate inflammation
*if damaged secrete prostaglandins (vasodilation) and adhesion molecules (extravasation = it refers to the movement of white blood cells from the capillaries to the tissues surrounding them (diapedesis). ) |
|
|
Term
| After particle is engulfed in phagosome... |
|
Definition
*joins with lysosome to become phagolysosome
*degradtion of particle may/may not be dependent on OXYGEN
*O2-dependent : NADPH mediates pdtion reactive oc=xygen species
*Oxygen-indep. = release granules containing proteolytic enzymes : defensins, lysozyme, cationic proteins causes degradation of particle |
|
|
Term
|
Definition
*it may present antigen to adaptive immune
*piece of digested particle will be put on receptor and taken to the surface of phagocyte
*then phagocyte will travel through lymphatics to lymph node and present to the adaptive immune system |
|
|
Term
|
Definition
*part innate (important) and adaptive
*biochemical cascade of 20+ proteins that combine and cleave(becomes activated) to stimulate adaptive immunity.
*C3 is the merge point of all pathways |
|
|
Term
| Basic functions of complement |
|
Definition
*lysis of cells (gram neg bact, viruses, fungi)
*opsonization: stickes to Ag, promotes phagocytosis
*chemotaxis: calls immune cells to area of inflammation
*binding to complement receptors to trigger cell functions, inflammation, immunoregulation
*immune clearance: removes Ag-Ab immune complexes in spleen and liver |
|
|
Term
| Three functions of complement |
|
Definition
(1) Host defense (innate get rid of early on), lysis of pathogens
(2) disposal of waste
(3) regulation of immunity |
|
|
Term
| Host defense : Induction of inflammation in complement |
|
Definition
*C5a, C3a, C4a
-smooth mm contraction, increase vascular permeability
*3,5 = induce vascular adhesion molecules
*5 = activates leukocytes and induces chemotaxis
*causes mast cell mediator release
*massive mediator release cause syndrome similar to anaphylaxis |
|
|
Term
| Host defense : opsonization in complement |
|
Definition
*any molecule that binds to a foreign Ag and enhances phagocytosis (coat w/ protein to neutralize charge so mac gets close)
*both mac and bacterial membranes have neg charge so opsonin bound to Ag gives the mac something to hang onto |
|
|
Term
|
Definition
*opsonin binds to the bacteria
*phagocytic cells have complement receptors and Fc receptors that recognize and bind the opsonin |
|
|
Term
Disposal of waste in complement
Regulation of the immune response |
|
Definition
*immune complex removal,apoptotic cell debris
*complement receptors on B and T cells can help to activate adaptive immunity by stimulating B and T cells |
|
|
Term
|
Definition
| *proenzyme or inactive enzyme precursor that has to be activared by hydrolysis to modify the enzyme to make it active |
|
|
Term
|
Definition
| *collection of complement proteins that assemble together w/i bacterial membrane to from a pore then pokes holes in the bacteria to lyse it |
|
|
Term
| Three complement pathways |
|
Definition
| *classical, alternative, mannose-binding lectin pathway |
|
|
Term
|
Definition
*requires Ab for activation
*only surface bound IgG and IgM can activate
*C1 made of q(6),r(2),s(2)
*C1q binds to org. starts cascade
*convertase is C4b2a = perpetuates proc. |
|
|
Term
|
Definition
*does not require Ab, can be activated by C3 hydrolyis (spontaneous cleavage) or Ag w/o Ab (nonspecific immune response)
*begins w/ spontaneous cleavege C3 to C3b, C3b ilmost instantly hydro. (destroyed) if doesn't bind to pathogen
*this cleaves C5 then C5b initiates MAC (C5b-6789) |
|
|
Term
| Mannose-binding lectin complement |
|
Definition
*not require Ab, can be activated by C3 hydrolysis or Ag w/o Ab
*soluble glycoprotein, binds mannose on certain pathways then activated at C3
*different from classical b/c starts w/ lectin binding to mannose on the bact/virus |
|
|
Term
| In all three complement pathways (C3) |
|
Definition
| *C3 protein is hydrolyzed by C3 convertase to make C3a and C3b causing complement cascade |
|
|
Term
| Specific complement component effects |
|
Definition
*chemotaxis (primarily phagocytes) = C3a
*mast degrn. = increased vascualr permeability, C5a, C3a
*contraction of smooth muslce = 5,3
Lysis = MAC-C5b initiated formation MAC |
|
|
Term
|
Definition
*initiator of classical comp. system
*6 legs of c1q bind to antigen
*old so rarely get deficiencies |
|
|
Term
|
Definition
*puts the brakes on!
*prevents C1R2S2 from being proteolytically active
*usually have problems with this one, causes overdoing of the comp. system |
|
|
Term
| Activation of complement - Lectin Path |
|
Definition
*lectin binds to carb structures
* |
|
|
Term
|
Definition
*osmotic gradient favors water movement into the cell, to survive the cell pumps out the water, excessive pores cause water flow into the cell
*membrane cant take the increased osmotic pressure so it ruptures |
|
|
Term
| Hereditary Angioedema (HAE) |
|
Definition
*rare, autosomal dominant
*C1 esterase inhibitor deficienct
*spontaneous angioedema (face, oral, resoiratory, cutaneous, GI)
*not IgE mediated (not allergic)
*overabundance of complement |
|
|
Term
|
Definition
*quanitative or qualitative, low levels during inflammatory conditions due to consumption of certain comp/ components (pdtion maxed out) or lack of pdtion
*comp. consumption as marker of disease
*used to diagnose angioedema, recurrent microbial infections, or chronic autoimmune disease or unexplained things |
|
|
Term
|
Definition
*can be proteins (mostly)
*some enter from outside (exogenous)
*other are inside (endogenous) |
|
|
Term
| Exogenous antigen processing |
|
Definition
| *taken up by APCs, these engulf by endocytosis, endosome fused w/ lysosome, antigen degraded into fragments, these displayed on surface nestled in receptors called class II HMC, are recognized by naive CD4 helper T cells |
|
|
Term
|
Definition
*each T cell receptor is specific for a particular seq of amino acids in an antigen
*selected in the thymus
*specific to antigen and specific to SELF-MHC
*antigen generated from proteins in digested in the APC
*Peptide is recognized in form when bound to an MHC molecule |
|
|
Term
| How intracellular virus get expressed on class I MHC? |
|
Definition
*viral proteins are degraded in phagolysosomes in the cytosol into antigens, picked up by TAPs (transporter assoc. with antigen processing)
*takes antigen to the ER, there they assemble with clss I MHC , then complex is recognized by cytotoxic T cells (CD8) who destroys then infected cell |
|
|
Term
|
Definition
*class I and II pathways can interconnect
*transferring exogenous antigens to class I pathway
*important b/c most viruses infect cells other than APCs, viruses
displayed on surface
*some viruses evade immune system so class I pathway needs help sp virus makes cell so can't put flag up, APC can help stimulate cell mediated immunity and present an antigen on class II, tells helper T cells that its not activated but another cell is. |
|
|
Term
|
Definition
*mechanism for cells to transfer endogenous antigens into the class II pathway.
*self-proteins are eaten, CD4 helper T cells that have receptors that recognize self-antigens are deleted to reduce autoimmunity, proteins syn. by an infecting virus can stimulate CD4 andCD8 T cells |
|
|
Term
|
Definition
| *can be both antigen presenting and antigen-receiving cells |
|
|
Term
|
Definition
*class of Ag which causes non-specific activation of T cells resulting in polyclonal T cell activation and MASSIVE cytokine release
*up to 20% of body's T cells activated |
|
|
Term
|
Definition
*aka ontogenesis or morphogenesis
*describes origin, growth, development from immature to mature form
*T lymphocytes originate in bone marrow, schooled in thymus, reside in secondary lymphoid organs or circulate in the blood until activated |
|
|
Term
|
Definition
*immune response genes are located in the MHC
*control T cell help and suppression
*peripheral effects : peptide binding
*central effects : selection in thymus |
|
|
Term
|
Definition
*maturation is Ag dependent
*TCR = binds w/ MHC for lymphocyte activation
*CD3 = part TCR complex, helps with intracellular signalling
*CD4 or CD8 = co-receptor MCH II or I
*CD2 = adhesion molecule found on T cells and NK cells
*when leave thymus have CD4 or CD8 if not are NK cell |
|
|
Term
|
Definition
*multi-lobed, surrounded by capsule
*composed of cortex and medulla
*T cell precursors from cortex to medulla |
|
|
Term
| Sequence of T cell maturation |
|
Definition
*first T cell progenitors express CD2, then TCR genes rearrange
*if they bind self MHC pass pos selection
*CD3,4,8 is double pos
*If do not react to self-Ag pass neg
*choose CD4 or CD8 single pos |
|
|
Term
|
Definition
*migrate to corticomedullary junction
*encounter macrophages and APCs
*if bind self fail neg selection and die |
|
|
Term
|
Definition
| *present mainly at epithelial surfaces, and recognize lipid antigens and may recognize damages cells (heat shock protein) |
|
|
Term
|
Definition
*type of cytotoxic lymphocyte
*use perforin/granzyme - apoptosis
*do not express TCR or CD3
*do not have to be activated by binding MHC to kill abnormal cells (innate)
*can be activated by IFNs / cytokines
*can bind Fc portion of Abs to kill
*secrete IFN and TNF to upregulate |
|
|
Term
|
Definition
*contain T and B lymphocytes, and macrphages
*filter and trap foreign particles |
|
|
