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Immunology Flashcards

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1
Q

Immunity - define

A

Resistance exhibited by the host against any foreign antigen including microorganisms.

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2
Q

Types of immunity.

A
  1. Innate immunity→possesses by birth.
    a) species immunity→resistance to a pathogen by all members of a particular species.
    b) racial immunity→within one species different races exhibit difference in susceptibility / resistance to infection.
    c) individual immunity.→ resistance to infection varies withdifferent individuals of same race & species.
  2. Acquired immunity→ acquired by an individual during life
    a) active immunity
    - natural→ through clinical/ subclinical infection.
    - artificial → induced by vaccination.
    b) passive immunity
    - natural→ trough transplacental maternal IgG antibodies
    - artificial→through antiserum injection.
  3. Adoptive immunity→ injection of immunologically competent lymphocytes.
  4. Local immunity→ immunity at the site of entry.
  5. Herd immunity → overall resistance in a community
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3
Q

Mechanism of innate immunity.

A
  1. Epithelial surfaces
    a) skin
    b) respiratory tract
    c) intestinal tract
    d) conjunctiva.
    e) genitourinary tract
  2. Antibacterial substances →properdin, complement, lysozyme, betalysin, basic polypeptides & interferons.
  3. Cellular factors→ phagocytosis by macrophages & microphages
    a) chemotaxis
    b) attachment
    c) ingestion.
    d) intracellular killing
  4. Inflammation
  5. Fever
  6. Acute phase proteins.→c reactive protein, mannose binding proteins, etc.
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4
Q

Cells involved in innate immunity

A
  1. Microphages→polymorphonuclear leukocytes ( neutrophils)

2. Macrophages →mononuclear phagocytic cells

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5
Q

Live vaccines.

A 
→ BCG for tuberculosis.
→ Ty 21a for typhoid.
→ Sabin vaccine for poliomyelitis.
→ MMR vaccine for measles, mumps,rubella.
→ 17 D vacuum for yellow fever.
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6
Q

Killed vaccines.

A 
→ TAB for enteric fever.
→ killed cholera vaccine
→ Salk vaceue for poliomyelitis.
→ neural & non- neural vaccines for rabies.
→ hepatitis B vaccine
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7
Q

Vaccines from bacterial products.

A

→ tetanus toxoid for tetanus.

→diphtheria toxoid for diphtheria.

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8
Q

In killed vaccines organisms are killed by _

A

Heat, formalin, phenol & alcohol.

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9
Q

Agents used for artificial passive immunity

A

→ hyperimmune sera of animal/ human origin
→convalescent sera
→ pooled human gammaglobulin.

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10
Q

Features of passive immunity

A

→ received passively by the host. Host’s immune system does not participate.
→ conferred by administration of ready made antibodies.
→ protection short lived & less effective.
→ immunity is effective immediately.
→No immunological memory.
→ No negative phase
→ applicable in immunodeficient person.
→ used for treatment of acute infections

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11
Q

Haptens.

A

Substances unable to induce antibody formation on its own but can become immunogenic when covalently linked to carrier proteins.
→ complex haptens- combine with specific antibodies to form precipitates
→ simple haptens- combine with specific antibodies but no precipitate is produced.

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12
Q

Properties of antigen.

A
  1. Foreignness
  2. Size
  3. Chemical nature
  4. Susceptibility to tissue enzymes.
  5. Antigenic specificity
  6. Species specificity
  7. Isospecificity
  8. Autospecificity
  9. Organ specificity
  10. Heterophile specificity.
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13
Q

Heterophile antigens.

A

→ similar antigens shared by unrelated species. →eg. Forssman antigen
Weil- Felix reaction
Paul - Bunnell test

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14
Q

Antigen

A

A substance which, when introduced into a body evokes immune response to produce a specific antibody with which it reacts in an observable manner.

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15
Q

Antibody

A

Substances which are formed in the serum & tissue fluids in response to an antigen & react with that antigen specifically.

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16
Q

Different types of antibodies.

A

IgG, IgA, IgM, IgE, IgD

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17
Q

Immunoglobulin G.

A

→major serum Ig (80% of total amount)
→Normal serum concentration =8-16 mg/ml
→ MW= 150,000
→ 1/2 life = 23 days
→ only Ig transported through placenta provides natural passive immunity to newborn.
→equally distributed btw intravascular extravascular compartment.
→ appears late but persists for longer period
→ participates in precipitation, complement fixation neutralisation of toxin & viruses.
→ binds to microorganisms & enhances phagocytosis.
→catabolism depends on the serum IgG concentration
→ passive administration suppresses the homologous antibody synthesis by feedback mechanism.
→4 subclasses- Ig G1-4
→protective against microorganisms active in blood & tissues.

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18
Q

Immunoglobulin A

A

→ second major serum Ig ( 10- 13%)
→ Normal serum concentration = 0.6-4.2 mg/ml
→ 1/2 life= 6-8 days.
→ Two forms- serum ig A & secretory ig A.
→ MW = 160,000 & 400,000
→ Two monomer units joined together by a glycoprotein named J chain.
→secretory igA :J chain produced by plasma cells situated near mucosal/ glandular epithelium.
→secretory igA contains glycine rich polypeptide called secretory piece/component.
→ The s piece protect igA from Denaturation by bacterial proteases in intestinal mucosa
→ present in milk, saliva, tears, sweat, nasal fluids, colostrum, secretions of respiratory, intestinal & genital system.
→ covers microorganisms to inhibit their adherence to mucosal surfaces.
→ activate alternative complement pathway.
→2 subclasses- igA 1,2.

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19
Q

Immunoglobulin M.

A

→ Pentamer consisting 5 ig subunits & one molecule of J chain.
→ 5-8% of total serum ig
→ Normal serum level = 0.5-2 mg/ml.
→ 1/2 life = 5 days.
→ Mw = 900,000-1,000,000 ( millionaire molecule).
→ mainly intravascular distribution (80%).
→ earliest synthesised ig by foetus in 20 weeks.
→ appears early in response to infection before igG.
→presence in serum indicates recent infection.
→ cannot cross placenta
→ presence in serum of newborn indicates congenital infection.
→ useful for the diagnosis of congenital syphilis, HIV, toxoplasmosis &, rubella.
→ effective in agglutination,complement fixation, opsonisation, & immune haemolysis.
→protection against blood invasion by microorganisms.
→ deficiency associated with septicaemia
→ appears on the surface of unstimulated B lymphocytes & acts as recognition receptors for ag
→2 subclasses- ig M1,2

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20
Q

List antigen-antibody reactions.

A
  1. Precipitation reactions
    a) ring test
    b) flocculation test
    →slide test
    → tube test.
    c) immunodiffusion test
    → single diffusion in 1D( oudin method)
    → double diffusion in 1D( Oakley- fulthorpe method)
    → single diffusion in 2D (radial immunodiffusion)
    → double diffusion in 2D(ouchterlony method)
    → immunoelectrophoresis
    → electroimmunodiffusion
    -counterimmunoelectrophoresis
    -rocket electrophoresis.
    -laurell’s 2D electrophoresis
  2. Agglutination
    a)slide agglutination test
    b)tube agglutination test
    c) Antiglobulin/ Coombs test
    d) Heterophile agglutination test
    → Weil - Felix reaction
    →Paul- Bunnel test
    →streptococcus MG agglutination test.
    e) passive agglutination test
    → latex agglutination test
    → hemagglutination test
    → coagglutination.
  3. Complement fixation test
  4. Conglutination
  5. Neutralization test
    a) in vivo tests
    →toxigenicity test
    → shick test
    b) in vitro tests
    → antistreptolysin O test
    → virus neutralization test
    → Nagler reaction
  6. Opsonisation
  7. Immunofluorescence
    a) direct Immunofluorescence test
    b) indirect Immunofluorescence test
  8. Radioimmunoassay
  9. Enzyme linked immunosorbent assay
    a) sandwich ELISA
    b) indirect ELISA
    c) competitive ELISA
    d) cassette /cylinder ELISA
  10. Immunochromatography
  11. Chemiluminescence assay
    12.immunoelectronmicroscopic tests
    a) immunoferritin test
    b) immunoelectronmicroscopy
    c) immunoenzyme test
  12. Immunoblotting
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21
Q

Prozone phenomenon.

A

Absence of precipitation (false negative) in the presence of excess antibodies is knower as Prozone phenomenon.

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22
Q

Radial immunodiffusion/ single diffusion in 2D- use.

A

Used for quantification of immunoglobulin classes.

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23
Q

Double diffusion in 2D - use.

A

Used for studying relation between antigens.

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24
Q

Eg of ring precipitation.

A
  1. Lancefield’s sero grouping

2. Ascoli’s thermoprecipitation test

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25
Q

Eg of slide precipitation.

A

VDRL

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26
Q

Eg of tube precipitation.

A

Kahn test

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27
Q

Precipitation reactions - principle.

A

Soluble antigen + specific antibody → • electrolytes• desired temperature ⇒ precipitation (settles down), flocculation ( floats)

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28
Q

Agglutination reaction- principle.

A

Particulate antigen + specific antibody → electrolytes, desired temperature ⇒ agglutination/clumping

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29
Q

Precipitation reaction is more sensitive for defection of _

A

Antigen

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30
Q

Agglutination reaction is more sensitive for detection of _

A

Antibody

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31
Q

Slide agglutination uses

A

→ identification of bacterial pathogens.
→ blood grouping
→cross matching.

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32
Q

Tube agglutination test- uses.

A
  1. Serological diagnosis of:
    → enteric fever ( Widal test)
    → typhus fever ( weil-felix reaction)
    → infections mononucleosis ( Paul-bunnel test)
    → brucellosis
  2. Diagnosis of 1° atypical pneumonia ( streptococcus MG agglutination test)
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33
Q

Coombs test- principle

A

When sera containing incomplete anti - Rh antibodies are mixed with corresponding Rh positive RBC’s, the incomplete antibody globulin coats the RBC’s but no agglutination occurs. When such coated RBC’s are treated with antiglobulin/ Coombs serum, the cells are agglutinated.

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34
Q

Coombs serum content.

A

Rabbit antiserum against human gamma globulin.

35
Q

Coombs test-uses.

A
  1. Direct Coombs test - erythroblastosis fetalis ( due to Rh incompatibility)
  2. Indirect Coombs test- paternal testing for Rh abs
  3. For demonstration of any type of incomplete antibody eg. Brucellosis.
36
Q

Heterophile agglutination test - principle.

A

Heterophile antibodies have a property to react with microorganisms / cells of unrelated species due to common antigenic sharing.

37
Q

Weil - Felix reaction

A

Some proteus strains ( OX 19, OX 2, OXK) are agglutinated by sera of patients with rickettsial infections due to antigenic sharing btw them.

38
Q

Passive agglutination test - principle.

A

Soluble antigen coated onto a neutral carrier ( sheep RBC’s, gelatin, latex, bentonite particles) ⇒ particulate antigen.

39
Q

Fluorochromes used in immonofluorescent assays.

A
  1. FITC ( fluorescein isothiocyanate)

2. Lissamine shodamine.

40
Q

Direct immunoftuorescence test -principle

A

Monoclonal antibodies specific to antigen → added to specimen → washed & observed under fluorescent microscope.

41
Q

Direct immunoftuorescence test - uses.

A

→ detection of bacteria, viruses or other antigens in blood, CSF, urine, faeces, tissues & other specimens
→ sensitive method to diagnose rabies

42
Q

Indirect immonofluorescence test- principle.

A
  1. For antibody detection: patients serum is added to slides precoated with antigen → add sheep/ goat antihuman antibodies + FITC → Wash & observe under fluorescent microscope.
    Eg. Antibody detection in serum of syphilis patient.
  2. For antigen detection: antibacterial antibody ( unlabelled) made in rabbit + antigen →+ anti-rabbit ig, labelled with fluorescent dye → observe
43
Q

Enzyme → substrate → chromogen- used in ELISA

A
  1. Horseradish peroxidase→ hydrogen peroxide → tetra-methyl benzidine.
  2. Alkaline phosphatase → p-nitro phenyl phosphate → p-nitro phenyl phosphate.
44
Q

Direct ELISA

A
  1. Used for antigen detection.
  2. Patients specimen coated to the well of ELISA plate → add monoclonal antibodies specific to antigen + conjugated with enzyme → wash after some time→ if specimen contains antigen → enzyme bring colour change
  3. Very poor sensitivity.
45
Q

Indirect ELISA

A
  1. Used for antibody detection.
  2. Anti HIV antibodies containing serum is added to antigen precoated plate → wash → sheep/ goat antihuman ig + enzyme → add substrate → look for colour change.
46
Q

Sandwich ELISA

A
  1. Used for antigen detection.
  2. ELISA plate containing wells coated with capture antibodies ie. sheep anti rota virus → wash → defector antibodies( rabbit antirotavirus antibodies)→ conjugated with enzyme → substrate added → look for colour change.
47
Q

Uses of ELISA

A
  1. Detection of HIV antibodies in serum.
  2. Detection of mycobacterial antibodies in tuberculosis.
  3. Detection rotavirus in faeces.
  4. Detection of hepatitis B markers in serum.
  5. Detection of enterotoxin of E.coli in faeces.
48
Q

Monoclonal antibodies are produced by _ cells.

A

Single clone of B cells

49
Q

Monoclonal antibodies are produced using _ technology

A

Hybridoma

50
Q

Properties of plasma cells extracted from the spleen of mouse in hybridoma technology.

A

→ Ig +
→ HGPRT enzyme +(Hypoxanthine-guanine phosphoribosyltransferase)( salvage pathway of purine synthesis)
→short 1/2 life.

51
Q

Properties of genetically modified myeloma cells fused with plasma cells extracted from the spleen of mouse in hybridoma technology.

A

→ Ig -ve
→ HGRPT enzyme -ve
→ indefinite 1/2 life ( desirable property)

52
Q

Fusion of plasma cells with myeloma cells is done by which techniques.?

A
  1. Polyethylene glycol.
  2. Inactivated Sendai virus → non pathogenic virus → paramyxovirus containing fusion protein.
  3. Electrofusion.
53
Q

After fusion which cells are produced in hybridoma technology.?

A
  1. Hybridoma cells → Abs +ve, HGPRT enzyme +ve, indefinite 1/2 life.
  2. Unfused plasma cells → die eventually due to short 1/2 life.
  3. Unfused myeloma cells → indefinite 1/2 life
54
Q

Which medium is used to kill unfused myeloma cells.?

A

HAT medium
• hypoxanthine]→ substrate for
• thymidylate. ] salvage pathway.
• aminopterine → inhibits the denovo pathway.

55
Q

Hybridoma cells are maintained in_

A

Cell lines, mouse peritoneal cavity.

56
Q

Application of monoclonal antibodies.

A
  1. Diagnostic use
    → identification of bacterial, viral & other antigens.
    → as conjugates in direct fluorescence & enzyme linked assays.
  2. Pure antibody
57
Q

Disadvantages of monoclonal antibodies.

A

Cannot be used for the treatment of human disease since they are derived from mouse plasma cells → Act as foreign antigen → induce Human Anti Mouse Antibody Response.

58
Q

Biological functions of complement.

A
  1. Bacteriolysis & cytolysis.
  2. Amplification of inflammatory response.
  3. Hypersensitivity reactions. →type 2( cytotoxic) & type 3 ( immune complex)
  4. Endotoxic shock
  5. Immune adherence
  6. Opsonisation → facilitated phagocytosis
  7. Autoimmune diseases
59
Q

Antibodies activating classical complement pathway.

A

Ig M > IgG3 > IgG 1> IgG2

60
Q

Alternative complement pathway aka _

A

Properdin pathway

61
Q

Alternative complement pathway activated by?

A

Lipopolysaccharide, viral envelopes, fungal walls, cobra venom, IgA/IgD aggregates, nephritic factor

62
Q

List complement deficiencies.

A
  • c1, c2,c4→ SLE
  • c3→ severe pyogenic infections.
  • MBL → severe pyogenic infections
  • c5, c6,c7, c9 →predisposition to neisseria infections
  • c1 esterase→ hereditary angio neurotic edema
  • DAF & CD 59 → paroxysmal nocturnal hemoglobinuria
63
Q

Complications of blood transfusion.

A 
1. Immunological complications
→ incompatible blood transfusion
→ intravascular haemolysis
→ Extravascular lysis
→hypersensitivity to some allergens in donor blood.
2. Non - immunological complications
      a)viruses
         → HIV-1 & HIV-2
         → hepatitis B, C & D viruses
         →cytomegalovirus
      b) bacteria
          → treponema pallidum
          → leptospira interrogans
       c) Protozoa
           → Plasmodia
           → leishmania donovani
           → toxoplasma gondii
64
Q

The allograft reaction.

A

→ Rejection of the graft by the recipient
→ first set response → by 10th day
→ due to cell mediated reaction
→ 1° rejection by helper T lymphocytes → activates cytotoxic T lymphocytes, macrophages & B lymphocytes
→ second set response→ by 6th day
→ mainly by antibodies along with cell mediated immunity

65
Q

Mechanism of autoimmunity

A
  1. Hidden or sequestered antigens→ lens antigen of eye, sperm & thyroglobulin
  2. Antigen alteration→ by physical, chemical or biological factors → neoantigens
  3. Cross reacting foreign antigens →streptococcus M protein & heart muscles
  4. Forbidden clones→clone of cells carrying a pattern reactive against self antigens
  5. T & B cell defects→enhanced function of T helper cell & decreased T suppressor cell function
66
Q

1° immunodeficiency syndromes

A
  1. Humoral immunodeficiencies (B cell defects)
    → X-linked agammaglobulinaemia
    → transient hypogammaglobulinaemia of infancy
    → common variable immunodeficiency
    → selective immunoglobulin deficiencies
    → immunodeficiencies with hyper-IgM
    → transcobalamin 2 deficiency
  2. Cellular immunodeficiencies (T cell defects)
    →Thymic hypoplasia ( DiGeorge’s Syndrome)
    → purine nucleoside phosphorylase ( PNP)deficiency
  3. Combined immunodeficiencies (Both B&T cell defects )
    → cellular immunodeficiency with abnormal immunoglobulin synthesis( Nezelof’s syndrome)
    → ataxia telangiectasia
    → Wiskott- Aldrich syndrome
    → immunodeficiency with thymoma
    → severe combined immunodeficiency diseases
    → MHC class 2 deficiency
  4. Disorders of complement
    → complement component deficiencies
    → complement intribitor deficiencies
5. Disorders of phagocytosis
→chronic granulomatous disease
→ myeloperoxidase deficiency
→ Chediak - Higashi syndrome
→Leucocyte G-6-PD deficiency
67
Q

List the cells of lymphoreticular system.

A
  1. Lymphocytes
    a) T- lymphocytes
    → T helper ( CD4) cells
    →T suppressor ( CD8) cells
    → cytotoxic T ( Tc) cells
    → delayed type hypersensitivity (DTH) cells
    → mixed lymphocyte reactivity (MLR) cells.
    → CD2, CD3, CD4, CD5, CD8
    b) null cells
    → killer cells
    → natural killer cells
    → lymphokine activated killer cells.
    c)B -lymphocytes & plasma cells.
  2. Phagocytic cells
    a) macrophages
    b) Microphages
    →neutrophils
    → eosinophils
    → basophils

3.dendritic cells

68
Q

Functions of macrophages.

A
  1. Phagocytosis
  2. Specific immune response.
    a) MHC restriction
    b) IL -1 from activated macrophages.
  3. Antitumour activity & graft reduction.
69
Q

Major histocompatibility complex.

A

→ aka Human Leukocyte Antigen (HLA) complex.
→ MHC locus: short arm of chromosome 6
→ class 1 & 2: most polymorphic genes.
• class 1: B >A>C
• class 2: most polymorphic: HLA DR beta
least polymorphic: HLA DR alpha.
→ class 3 region: conserved genes encodes: c2, c4, complement protein, factor B, TNF alpha + beta, heat shock protein.

→ class 1 MHC antigen:
• expressed on the surface of all nucleated cells + platelets
• encoded by HLA- A, B,C gene loci
•function: presenting endogenously synthesised peptides / cytosolic peptides to cytotoxic T cells.
• structure:
- polymorphic alpha chain
- conserved beta2 microglobulin
- peptide presenting groove btw alpha1 & alpha2
- 8-10 amino acid peptides.
• assembly in endoplasmic reticulum.

→class 2 MHC antigen:
• expressed only on antigen presenting cells ( APCs)
• encoded by HLA - DP, DQ, DR gene loci.
•function: presenting peptides of exogenous antigens / extracellular pathogens to helper T cells.
• structure:
- polymorphic alpha chain
- polymosphie beta chain
- peptide presenting groove btw alpha1 & beta1
- 13-25 amino acid peptides
• assembly in endosome

70
Q

HLA- role in immunity.

A

Cell surface antigens that evoke immune response to an incompatible host resulting in allograft rejection. These alloantigens are present on surface of leuckorytes in man known as HLA

71
Q

HLA typing.

A

→ Antisera from multiparous women are collected for HLA typing
→ typing is done serologically by complement dependent cytotoxic reaction.
→ lymphocytes of donor is typed against recipient sera in the presence of complement
→ serological typing is not possible for HLA-D & HLA-DP antigens.
→ HLA-D detected by mixed leucocytic reaction
→ HLA-DP detected by primed lymphocyte typing
→ indications:
1. Tissue typing prior to transplantation.
2. Paternity determination.
3. Diseases & HLA association.
• HLA-B27: ankylosing spondylitis
• HLA-DR4: rheumatoid arthritis.

72
Q

Lymphoid organs.

A 
1. Central/ 1° lymphoid organs.
     thymus→produce thymic lymphocytes.
     bursa of Fabricius in birds
     bone marrow in mammals.→ stem cell proliferation, origin of pre-B cells & their maturation into functional B-lymphocytes.
2. Peripheral/ 2° lymphoid organs.
     spleen
     lymph nodes
     mucosa associated lymphoid tissue
     lymphoid tissue in gut, lungs, liver, bone marrow
73
Q

T helper cells ( cd4)

A

→ 65% of circulating T-lymphocytes.
→ Th1 produce cytokines such as interferon gamma & IL-2 which activate macrophages & T cells to promote cell mediated immunity.
→ Th2 interact with B-lymphocytes fo develop them into plasma cells that produce immunoglobulins.
→ overactivity → autoimmunity
→ decreased function → immunodeficiency.

74
Q

T cell v/s B cell

A

Feature T cell B cell
• thymus specific antigens + -
• CD3 receptor + -
• surface immunoglobulins - +
• receptor for Fc fragment of IgG - +
• SRBC rosette ( E-rosette) + -
• EAC rosette (C3 receptor) - +
• numerous microvilli on surface - +
• blast transformation with:
1. Anti -CD3 + -
2. Anti-Ig - +
3. Phytohaemagglutinin + -
4. Concanavalin A. + -
5. Endotoxins - +
• peripheral blood 65-85 % 15-25%

75
Q

B cells.

A

→ Both antigen receiving & antigen presenting cell to helper T cells.
→ bind intact antigen with their B cell receptors.
→ comes in contact with antigens during peripheral circulation or presented by dendritic cells
→ B cells take up antigen by receptor-mediated endocytosis. ⬇️
Antigen cleaved into multiple peptides.
⬇️
Peptides displayed on cell surface in groove of MHC class 2 molecules
⬇️
CD4+ T cell recognises displayed peptides.
⬇️
Stimulate the release of lymphokines
⬇️
Stimulate B cell to enter cell cycle.
⬇️
Plasma cells formed.
⬇️
Secrete antibodies with specificity
→ memory B cells circulate in blood & reside in mucosal & other tissues.

76
Q

Natural killer cells.

A

→large lymphocytes containing azurophilic granules in the cytoplasm, aka large granular lymphocyte (LGL).
→ NK cells are cytolytic for virally transformed target cells, certain turnout lines & are involved in allograft rejection.
→ found in spleen & peripheral blood.
→ action independent of antibody.
→their activity is natural & nonimmune as it does not require sensitisation by prior antigenic contact.
→ activity is enhanced by interferon
→ important role in antiviral & antitumour immunity.

77
Q

Macrophages.

A

→ blood macrophages (monocytes) are the largest of the lymphoid cells in peripheral blood.
→ tissue macrophages (histiocytes) are named as alveolar macrophages in the lungs & kupffer cells in liver
→ tissue macrophages proliferate locally
→ express surface receptors: Ia proteins, for the Fc part of IgG, activated complement components & various lymphokines.

78
Q

Cell mediated immunity

A

→specific acquired immune responses mediated by sensitised T cells.
→ can be transferred from donor to recipient with intact lymphocytes.
→ imp role in immunological functions:
1. Delayed hypersensitivity (type4)
2. Immunity in infectious diseases caused by intracellular organisms.
3. Transplantation immunity & graft-versus-host reaction.
4. Immunological surveillance & immunity against cancer
5. Pathogenesis of certain autoimmune diseases eg. Thyroiditis
→ foreign antigen presented by antigen presenting cells to T-lymphocytes
⬇️
T cell receptors recognise foreign antigen & a self MHC molecule on the surface of APC
⬇️
Sensitised T- lymphocytes undergo blast formation, clonal proliferation & differentiation into memory cells & effector cells (Th, Tc, Td & Ts)
⬇️
Activated lymphocytes release biologically active products ( lymphokines) which manifests CMI
→T cells recognise antigens only when presented with MHC molecules.
→CD8+ cells: recognise the combination of foreign antigen & class 1 MHC antigen & differentiate into Tc & Ts lymphocytes.
→CD4+ cells: recognise the combination of foreign antigen & class 2 MHC antigen & differentiate into Th & Td lymphocytes.
→ Tc lymphocytes: recognise foreign antigen & class 1 MHC antigen & gets attached to the target cell.
→Tc lymphocytes release cytolysins which leads to lysis of the target cell.
→ detection:
1. Skin tests for delayed hypersensitivity.
2. Lymphocyte transformation test.
3. Migration inhibiting factor test.
4. Rosette formation.
5. Detection of T-cells by immunofluorescence technique

79
Q

Cytokines

A

→ biologically active substances secreted by monocytes, lymphocytes & other cells.
→ lymphokines from lymphocytes.
→ Monokines from monocytes & macrophages.
→ interleukins are chemical substances that function 1°ly as growth & differentiating factors.
→ Not specific for antigens.
1. Interleukins: 1-18.
2. Colony stimulating factors: G-CSF, M-CSF.
3. Tumour necrosis factors: alpha & beta
4. Interferons: alpha, beta & gamma.

80
Q

Adjuvants.

A

→ any substance that enhances the immunogenicity of an antigen.
→types:
1. Depot: aluminium hydroxide/ phosphate, alum & Freund’s incomplete adjuvant ( water in archis oil)
2. Bacterial: Freund’s complete adjuvant = Freund’s incomplete adjuvant + suspension of killed tubercle bacilli.
3. Chemical: bentonite, calcium alginate & silica particles.
→ actions:
1. Sustained release of antigen from depot
2. Stimulate lymphocytes non-specifically
3. Activate macrophages
4. Stimulate CMI

81
Q

Interleukins.

A
  1. IL-1 →stimulation of T cells for the production of IL-2 & other lymphokines,B cell proliferation, neutrophil chemotaxis.
  2. IL-2 → major activator of T & B cells, cytotoxicity of T & NK cells, helps in destruction of tumour cells.
  3. IL-3 → acts as a growth factor for bone marrow stem cells
  4. IL-4 → proliferation of B & cytotoxic T cells, augments IgE synthesis.
  5. IL-6 → induces immunoglobulin synthesis by B cells, formation of IL-2 receptors on T cells.
82
Q

Hypersensitivity

A 
→A condition in which immune response results in excessive reactions leading to tissue damage, disease or even death in sensitised host.
→ 2 types: immediate & delayed.
→ coomb & gel classification:
     type 1- anaphylactic
     type 2- cytotoxic
     type 3- immune complex
     type 4- delayed/ cell mediated
     type 5- stimulatory type
83
Q

Type 1/ anaphylactic reaction.

A

→2 forms: anaphylaxis & atopy.
→anaphylaxis occurs when a sensitised individual comes in contact with a shocking dose of antigen.
→most effective route for sensitisation is parenteral.
→during sensitisation (2-3 weeks), cytotropic antibody IgE is produced against the antigen attaches to surface receptors of mast cells and basophils.
→when a shocking dose of same or immunologically related antigen is given, the antigen combines with cell bound IgE antibody on mast cells rapidly.
→the antigen-antibody complex stimulates mast cells and basophils to release meditators that cause clinical manifestations of anaphylaxis.

84
Q

Chemical mediators of anaphylaxis

A
  1. Primary mediators- preformed contents of mast cell and basophils granules.
    a) histamine-vasodilation, increased capillary permeability and contraction of smooth muscles.
    b) serotonin-vasoconstriction, increased capillary permeability, smooth muscle contraction.
    c) eosinophil chemotactic factor of anaphylaxis(ECF-A)
    d) proteolytic enzymes- proteases and hydrolases
  2. Secondary mediators- newly formed upon stimulation of mast cells, basophils and other leukocytes
    a) slow reactions substance of anaphylaxis- bronchoconstriction of asthma.
    b) prostaglandins & thromboxane- bronchoconstrictor.
    c) platelet activating factor
    d) other mediators of anaphylaxis- anaphylatoxins, bradykinin,etc.

Microbiology (7 decks)

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