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A.  Abnormal immune response which produces physiological/ histopathological damage in the host


Type I Anaphylactic: IgE mediated
Type II Cytotoxic
Type III Immune complex arthus/serum sickness
Type IV Delayed: T- cell mediated
Type V Stimulatory/ Antireceptor

Immediate type : I, II, III,V (< 24 hrs)


Delayed type : IV (24 -48 hrs)


1.  Type I hypersensitivity (Anaphylaxis)

  1. Mediated by IgE and mast cells
  2. Local/ generalized
  3. Local (Hay fever, asthma)
  4. Systemic (shock life condition) venom, penicillin, horse serum

a.  Prausnitz - Kustner (PK) reaction

  1. serum from allergic person into skin of normal person
  2. Serum from anaphylactically sensitized person to (I/D) skin of normal person
  3. After 48 hrs challenged with allergen and Evans blue dye (I/V)
  4. Blueing of site of I/D injection (area proportional to quantity of IgE present in the serum)

b.  Anaphylaxis in vitro (Schultz-dale)

  1. Strips of smooth muscle contract in vitro following exposure to antigen

c.  Atopy

Chronic human allergic states (Hay fever, asthma, food allergies)

Principal mediators involved in type I hypersensitivity





Histamine, heparin

Increased vascular permeability; smooth muscle contraction

Serotonin (rodents)

Increased vascular permeability; smooth muscle contraction

Eosinophil chemotactic factor (ECF-A)

Eosinophil chemotaxis

Neutrophil chemotactic factors (NCF-A)

Neutrophil chemotaxis

Proteases (Tryptase, chymase)

Bronchial mucus secretion; degradation of blood vessel basement membrane; generation of complement split products.

Type II Hypersensitivity: Cytotoxic

  1. Combination of IgG and IgM with foreign antigenic components on a cell surface
  2. Complement - mediated cytotoxicity (Membrane attack complex, Phagocytes)
  3. Antibody- Dependent cell mediated cytotoxicity (ADCC)
  4. Drug induced immune hemolytic anaemia
    i.    Pencillin
    ii.    Methyl dopa
  5. Transfusion reactions
  6. Rh incompatibility
  7. Anaemia due to infections diseases

3.  Type III (Immune -complex mediated)

  1. Antigen soluble (not cell bound)
  2. Ag-Ab complex deposition in tissues
  3. Complement activation
  4. At equivalence (precipitation local reaction)
  5. Large Ag excess (systemic reaction)
  6. Arthus reaction (Local immune complex diseases)
  7. Serum sickness

                            i.    Horse antitoxin

  • Tetanus
  • Gas gangrene
  • Diphtheria

ii.    7-12 days after single dose

iii.    Lymphadenopathy, Fever, splenomegaly, arthritis, glomerulonephritis, endocarditis, vasculitis, nausea, vomiting


h. Pathogenesis in SLE and Rheumatoid arthritis


4.  Type IV or delayed /T-cell mediated

  1. Sensitized T- cells and macrophages
  2. 24-48 hrs after the presensitized host encounters Ag
  3. Tuberculin (infection type)
    1. 1-3 units of PPD/ tuberculin injected i/d
    2. In individual sensitised to tuberculoprotein
    3. Indurated reaction > 5mm within 48-72 hrs
    4. Erythema: due to ↑blood flow
    5. Induration : infiltration of mononuclear cells

Contact dermatitis type

  1. Chemicals (nickel, chromium ), dyes, drugs, (penicillin) come in contact with skin
  2. Not antigenic by themselves but acquire antigenicity on combination with skin proteins
  3. Subsequent contact: contact dermatitis
  4. Macules/papules/ vesicles/acute eczema

5.  TYPE V

  1. Antibody mediated
  2. Antibody reacts with a key surface component e.g. hormone receptor and stimulates the cell
  3. E.g.: Graves's disease and Myasthenia graves


A.  Shwartzmann reaction

  1. Not an immune reaction
  2. Culture filtrate of Gram –ve bacteria i/d rabbit
  3. After 24 hrs larger dose of same/ unrelated toxin i/v
  4. Within few hours at the site of i/d injection petechial haemorrhages are seen
  5. Absence of specificity, short interval
  6. Localized/ generalized (Waterhouse-Friderichsen syndrome) 

B. Immune response

  1. Specific reactivity following antigenic stimulus
  2. Humoral or antibody mediated
  3. Cell mediated immunity (CMI) 

C.  Humoral immune response

  1. Extracellular bacterial pathogens
  2. Viruses (respiratory/ intestinal)
  3. Hypersensitivity I, II, II
  4. Antigens presented to immunocompetent cells by antigen presenting cells ( macrophages, dendritic cell [lymph node follicle, skin, thymus, lymphnode, spleen]
  5. These cells present antigen at cell surface
  6. Interact with immunocomponent B cells
  7. Clonal proliferation and blast transformaion
  8. Some B cells converted into memory cells
  9. Antibody production stimulated by TH2 cells

D. Monoclonal antibody

  1. Normal antibody response: polyclonal
  2. Antibodies produced by a single clone and directed against single antigenic determinant
  3. Kohler and Milstein 1975, nobel prize
  4. Lymphocytes from mice spleen fused with mouse myeloma cells (deficient in HPRTase)
  5. Fused cells placed in medium containing hypoxanthine, aminopterin ,thymidine (HAT medium)
  6. Only fused cells grow
  7. These hybridomas can be grown in peritoneal cavity of mouse or tissue cultures 

E.  Cell Mediated Immune Responses

  1. Accomplished by effector T cells and macrophages rather than B cells and antibodies
  2. Protects against fungi, virus, intracellular bacterial pathogens (M.leprae, M.tuberculosis, Brucella, Salmonella), parasites (leishmania , trypanosomes)
  3. Allograft rejection,
  4. Delayed hypersensitivity
  5. Immunological surveillance
  6. Immunity against cancer
  7. Primary                   
  8. Initial contact   with foreign Ag
  9. Ag presented by antigen presenting cells to Tcell
  10. T cell receptor combines with foreign antigen along with self MHC molecule                         
  11. Proliferation of specific clones of effector T cells
  12. Secondary More pronounced, more rapid
  13. Memory cells 

F.  T cell differentiation

  1. Two modes of antigen processing
  2. Processing of phagocytosed material eg bacteria. The antigen is degraded and associated with class II    molecules. The antigen MHC II complex then expressed on the surface of antigen presenting cells
  3. Processing of antigens derived from within the cell (viral infection). Antigen MHC I complex expressed on cell surface
  4. CD8+ Tcells recognize ag in association with self MHC I
  5. CD4+ Tcells recognize ag in association with self MHC II

G. Cytokines

  1. Soluble mediators of host defence responses, both specific and non specific
  2. Same cytokine can be produced by multiple cell types and can have multiple effects on the same cell
  3. Small proteins(8-80KDa) usually acting in an autocrine or paracrine manner

H. Chemokines

  1. Chemoattractant cytokines
  2. Four major groups based on the cysteine structure near the amino terminus
    1. C: Lymphotactin
    2. CC: MIP α (Lymphoctes, monocytes, eosinophils, basophils)
    3. CXC: IL8 (neutrophils)
    4. CXXC: Fractalkine (Neutrophils, monocytes, T cells)

Transplantation Immunity

  1. Autograft : One part of body to another
  2. Isograft: B/W Genetically identical twins
  3. Allograft: B/W members of the same species but of different genetic constitution
  4. Xenograft : B/W members of different species 

I.   Allograft Reaction

1. Hyperacute Rejection

  1. Presence of antibodies against graft
  2. Prior blood transfusion, multiple pregnancies, previous transplant
  3. Preformed antibodies fix complement damaging endothelial lining of blood vessels (blockade) of microvasculature
  4. Time: Minutes to hours  

2. Acute Rejection / Accelerated Rejection

  1. Days to Weeks
  2. Primary Activation of T cells with Triggering of various effector mechanisms
  3. Transplant given to someone who has been presensitized 2o Activation of Tcells Accelerated /second set rejection (days)

3. Chronic Rejection

  1. Months to years
  2. Walls of blood vessel thicken and eventually become blocked
  3. Exact cause?
  4. Low grade cell mediated rejection
  5. Deposition of Ag – Ab complex
  6. Recurrence of original disease
  7. Main features
    1. Proliferation of smooth muscle cells
    2. Interstitial fibrosis
 J.   Major Histocompatibility Complex
  1. Genes mediating graft rejection
  2. MICE : called as H Loci
  3. Humans : Human leukocyte antigen complex
  4. Short arm of chromosome 6
  5. Co-dominantly expressed
  6. 4 Loci of HLA:  A,B,C,D
  7. 3 classes of Genes in these HLA loci  

1.  MHC class I

  1. HLA A,B,C
  2. Class I antigens
  3. 2 poly peptide chains
  4. Present in virtually all nucleated cells except RBCs
  5. CD8+ cells recognize Ag presented along with MHC I molecules  
  1. Encoded by HLA-DP, HLA-DQ, HLA-DR
  2. Two polypetide chains
  3. B lymphocytes, macrophages, monocytes, activated T lymphocytes  
  1. Genes coding for complement components C2, C4, properdin, factor B, TNFα, TNFβ,

Heat shock protein 70, Enzyme 21-hydroxylase

K. Graft Versus Host Reaction

  1. Occurs in bone marrow transplantation
  2. Induced by immunologically competent T cells being transplanted into allogenic recipients which are unable to reject them
  3. Due to lack of immuno-competence of host
  4. Severe damage to skin and intestine
  5. Potential complication after allogenic bone marrow transplantation

L.  Avoided by

  1. Careful typing
  2. Removal of mature T cells from graft
  3. Use of immunosuppressive drugs

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