Immunity - Immunology Serology PDF

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Summary

IMMUNITY – IMMUNOLOGY SEROLOGYImmunology – study of how a host’s body discriminate between self and foreign antigens and thereby eliminating these foreign substances. Immunity – state of being resistant to infections Tolerance – lack of immune response to self-antigensInnate/Natural/ Nonspecific Ada...

Description

IMMUNITY – IMMUNOLOGY SEROLOGY Immunology – study of how a host’s body discriminate between self and foreign antigens and thereby eliminating these foreign substances. Immunity – state of being resistant to infections Tolerance – lack of immune response to self-antigens Innate/Natural/ Nonspecific

Adaptive/Acquired/ Specific

CELLULAR

Antigen-presenting cells (eg. Dendritic cells) Phagocytes, eosinophils, basophils, mast cells NK cells

T-cells (T-cytotoxic and T helper) B-cells and plasma cells

HUMORAL

Lysozymes, Lactoferrin Acute phase reactants Complement, Properdin Pepsin, stomach acidity Cytokines (TNF, INF, beta-lysin

Antibod ies Cytokin es

RESPONSE

Rapid but short (less potent)

Slow but longer (more potent)

MEMORY

NO

YES (because of memory cells)

SPECIFICITY

General

Specific antigens

OTHERS

*with anatomical barriers – skin (pH 6.5), mucus membranes, normal flora, tears, cilia, saliva

INNATE IMMUNITY PHAGOCYTOSIS – process of engulfment of substances to be discriminated; done by cells called phagocytes

(1) Initiation

↓ (2) Chemotaxis

↓ (3) Engulfment

↓ (4) Digestion

↓ (5) Exocytosis

DIAPEDESIS – process in which blood cells pass through the intact walls of blood cells migrating to the site of injury

TWO FORMS OF PHAGOCYTOSIS Direct Phagocytosis

Indirect Phagocytosis Mediated by opsonins – antibodies (IgG/IgM), CRP, complement breakdown products C3b – most potent opsonin INFLAMMATION – cumulative mechanism (vascular and cellular) in respose to an injury or invasion by an infectious agent (1) Vascular Response

↓ (2) Cellular Response

↓ (3) Resolution and Repair

Cellular Response Acute infections: PMNs Chronic infections: Monocytes

CARDINAL SIGNS: Rubor – redness Calor – heat Tumor – swelling Dolor – pain Functio Laesa – loss of function ACUTE PHASE REACTANTS – serum proteins that significantly increase during course of an inflammation

APR

FUNCTION

INCREASE

RESPONSE TIME (hrs)

C-reactive protein

Opsonization

1000x

4-6

Serum Amyloid A

Cholesterol removal

1000x

24

Ceruloplasmin

Binds copper

2x

48-72

Complement C3

Opsonization, lysis

2x

48-72

Alpha1-antitrypsin

Protease inhibitor

2-5x

24

Fibrinogen

Clot formation

2-5x

24

Haptoglobin

Binds hemoglobin

2-10x

24

COMPLEMENT – proteins that are normally present in serum that has its functions during inflammation.

FUNCTIONS: For opsonization (C3b – most potent) For cell lysis (C5-C9 or MAC) Clearance of immune complexes

COMPLEMENT Protein

Function

Disease (if deficient)

C1q, r or s

C1q – binds Fc portion of IgG or IgM

Lupuslike syndrome

C1r – activation of C1s

Recurrent infections

C1s – cleaves C4 and C2 C4

Part of C3 convertase (C4b2a)

Lupuslike syndrome

C2

Binds to C4b to form C3 convertase of classical pathway

Lupuslike syndrome

(most common def.)

Recurrent infections

Atherosclerosis

C3

Pivotal point

(most sever def.)

C5b –C9

Severe recurrent infections

Glomerulonephritis

Part of Membrane Attack Complex

Neisseria infections

C8 – starts pore formation C9 – eventual cell lysis

No known disease

Factor B

Binds C3b to form C3 convertase

Factor D

Cleaves factor B

Properdin

Stabilizes C3bBb complex (C3 convertase of alternative complex)

Neisseria infections

MBL

Similar to C1q; binds to mannose

Pneumococcal diseases Sepsis Neisseria infections

MASP-1

Similar to C1r

MASP-2

Similar to C1s

Pneumococcal diseases

REGULATORY PORTEINS C1INH

Dissociates C1r and C1s from C1q thus inhibiting it

Hereditary angioedema

Factor I

Cleaves C3b and C4b

Recurrent pyogenic infections

Factor H

Cofactor of Factor I; inactivates C3b

C4-binding protein

Cofactor of Factor I; inactivates C4b

S-protein

Prevents the attachment of C5b67 to cell membrane

(vitronectin) DAF

Accelerates dissociation of both C3 convertases

MIRL ADAPTIVE IMMUNITY LYMPHOID ORGANS PRIMARY Thymus Atrophies as one ages Located in the thorax Site of T-cell maturation Bone Marrow Equivalent to Bursa of Fabricius in birds Site of hematopoiesis Site of B cell maturation SECONDARY Spleen – largest secondary lymphoid organ Tonsil Lymphoid tissues Peyer’s patches Appendix Mucosa-Associated Lymphoid Tissue (MALT)

Paroxysmal Nocturnal Hemoglobinuria

LYMPHOCYTES T CELL

B CELL

Cell-mediated immunity

Humoral-mediated immunity

Matures in thymus

Matures in bone marrow

60-80%

20-30%

CD4+ – T helper cells

Naive B cell

CD8+ – T cytotoxic cells

Activated B cell

T-regulatory cells

Plasma cell

Rosette formation identification

Identification by surface immunoglobulins (IgM and IgD)

CD2 – receptor for sheep RBCs

Lymphokines (products)

Antibodies (products)

CD2, CD3, CD4, CD8 antigens

CD19, CD20, CD21, CD40 and MHC Class II antigens

Located in the paracortex of lymph nodes

Located in the cortex of lymph nodes

Mitogens: Concanavalin A Phytohemagglutini n Pokeweed mitogen

Mitogens: LPS Pokeweed mitogen

FORMS OF ACQUIRED IMMUNITY

WHAT DID YOU ACQUIRE? If antigen → Active If antibody → Passive HOW DID YOU ACQUIRE? Naturally Artificially

ACTIVE

NATURAL

ARTIFICIAL

PASSIVE

Natural exposure to ANTIGEN

Natural exposure to ANTIBODIES

Ex. Recovery from infections

Ex. Colostrum, Transplacental

ANTIGEN was injected

ANTIBODIES were injected

Ex. Toxoids, Vaccinations

Ex. RhIg, anti-rabies, Hepatitis B Immune globulin, anti-tetanus

CYTOKINES – proteins that regulates immune system

PLEIOTROPY – single chemokine with different actions REDUNDANCY – different cytokines activate same pathways SYNERGY – acting in networks produing effects that complement & enhances each other...