• thymus
• lymph nodes
• spleen

• macrophages
• dendritic cells
• B cells (when present to helper T cell, become plasma cells)

• MHC II- exogenous nonself antigens
• MHC I- endogenous/intracellular antigens (aka viruses)

• MHC I- present to CD8 T cells
• MHC II- present to CD4 T cells

• helper T cell activation of B lymphocytes to synthesize specific Ab or direct cytotoxic T cell killing of virally infected cells

• ankylosing spondylitis
• postgonococcal arthritis
• acute anterior uveitis

• IDDM
• primary Sjogren syndrome
• chronic active hepatitis

• transfer across placenta
• secondary immunity

• binds to basophils and mast cells, sensitizing them

ADCC

• bind Fc receptor to Ab (usually IgG) which inturn is bound to target antigen
• usually involved in killing parasites, tumor cells, transplanted organ tissue

• exagerated response of one or more immune effector mechanisms causing harmful effect on the host
• function
  • provides protection from external environmental agents
  • sometimes elicits tissue damage
• ex: asthma, allergic rhinitis, transfusion reactions, drug reactions, transplant rejection, contact dermatitis

• anaphylaxis
• allergies
• bronchial asthma (atopic forms)

1. production of IgE Ab
2. cause immediate release of vasoactive amines and other mediates from mast cells
3. leads to recruitment of inflammatory cells (late phase rxn)

• pathology
  • vascular dilation
  • edema
  • smooth muscle conraction
  • mucus production
  • inflammation
• histology
  • edema
  • eosinophils
  • hyperemia

• autoimmune hemolytic anemia
• goodpasture syndrome
• transfusion reactions
• drug reactions
• hyperacute/acute rejection (ADCC type)

1. produce IgG, IgM
2. binds Ag on target cell or tissue ECM
3. phagocytosis or lysis of target cell by activated complement or Fc receptorsw
4. lead to recruitment of leukocytes

• pathology- cell lysis, inflammation
• histology
  • cell lysis
  • neutrophils
  • macrophages
  • fibrinoid necrosis (IgG, complement, fibrin)

• SLE
• glomerulonephritis
• serum sickness
• arthus reaction
• polyarteritis nodosa

1. deposition of Ag-Ab complexes (IgM, IgG, IgA) 
2. complement activation (C3a, C5a, C3b)
3. recruitment of leukocytes by complement products and Fc receptors
4. release of enzymes and other toxic molecules

• pathology
  • necrotizing fasculitis (fibrinoid)
  • inflammation
• histology
  • edema
  • neutrophils
  • fibrinoid necrosis
  • microthrombi

• contact dermititis
• MS
• IDDM
• transplant rejection
• TB test

1. activated T lymphocytes
   1. release of cytokines and macrophage activation
   2. T cell mediated cytotoxicity

• pathology
  • perivascular cellular inflitrates
  • edema
  • cell destruction
  • granuloma formation
• histology
  • macrophages
  • epitheloids macrophages
  • granulomas

mast cell

basophil

IgE

histamine

PG's

• cellular antigens
• complement activation
  • C3a
  • C5a
  • C3b
  • ADCC cell lysis

soluble Ag-Ab complexes

deposits

C3a, C3b, C5a

• cellular antigen T cell (helper and cytotoxic)
• cytokine release (IFN gamma, IL-2, TNF alpha, IL-12)

• happens within minutes of transplant
• happens when recipient has preformed antibodies directed against HLA antigens that immediately bound to grafted tissue (type II)
• pathology
  • within minutes, thrombosis with endothelial injury and necrosis becomes readily apparent
  • these are secondary to hemorrhage and infarction of the organ

• usually in vascular component (type II and some type III) or cellular (type IV)
• cellular type involves CD4, CD8, NK cellls
• both type II and IV are involved over course, but one may predominate over the other

• months following transplantation
• long term effects of cell mediated as well as Ab mediated immunity seen
• vascular changes
  • intimal fibrosis
  • secondary organ ischemia
  • fibrosis
  • atrophy
  • residual lymphocytic and plasmacytic infiltrate

• failure of peripheral tolerance
• fail central tolerance
• genetic factors
• microbial cause

NO TYPE I HYPERSENSITIVITY OCCURS IN AUTOIMMUNITY DISORDER

• endocrine
  • Hashimoto's thyroiditis (hypoT)
  • Grave's disease (hyperT)
  • IDDM

• autoAb's to thyroglobulin and thyroid microsomal Ag (enzyme thyroid peroxidase)
• others: anti TSH receptor antibodies

• lymphatic infiltration of thyroid gland
  • almost completely replace normal architecture

• lymphocyte infiltrate in thyroid gland
• this could lead to complete replacement of normal architecture

• antinuclear Ab's (directed against dsDNA)
• DNA histone complex
• ribonucleo-protein and nucleolus-specific RNA

• butterfly rash (exposure to UV light damage the skin, producing rash) with malar distribution
• decrease serum complement
• Ig deposits in skin, kidney
• renal involvment secondary to immune complex deposition in glomerular basement membrane

alternating exacerbations and remissions (predominantly affects females)