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Biomaterials Ch 12
The Acquired Immune Response
Undergraduate 2

Additional Engineering Flashcards




Properties of the Acquired Immune System

1) Specificity

2) Can respond to a diversity of antigens

3) Self/nonself recognition

4) Memory of previous invaders


Crossover between Innate and Acquired Immunity
Innate immune responses help form adaptive immune responses and adaptive immune responses utilize the machinery of innate immunity for effector function
Humoral Immune Response

B cell/antibody-mediated immune response; does not require antigen presentation


B cells mature in lymph nodes and spleen; co-stimulated by binding with antigens and secreted products from Th cells to fully activate the B cell


B cell clonal populations of effector (plasma cells containing soluble antibodies) and memory (contain membrane-bound antibodies, longer lifetime and more rapid/heightened response) develop

Cellular Immune Response

T cell/antibody-mediated immune response


T cells are formed in bone marrow and mature in the thymus


Antigen Presentation: Activation of T cells (binding between TCR and antigens)

T(h) cell pathway

Pathway for exogenous antigens


T(h) cells: express surface protein CD4


MHCII: Antigen binds to alpha and beta 1


antigens enter host cell through phagocytosis, degraded into peptide fragments during endocytosis


Fragments bind to MHCII molecules in endocytic vesicles, transported to cell membrane


T(h) cell produces cytokines that stimulate the humoral response, T(c) pathway


Common result of directly implanted biomaterial

T(c) cell pathway

Pathway for endogenous antigens (produced after alteration of a native cell due to toxic/carcinogenic properties of the biomatl)


Antigens first degraded into peptides w/in the cytoplasm, bind to MHCI in the RER, transported to cell membrane


MHC1- Express surface protein CD8; antigen binds to alpha 1 and 2 regions (found on all nucleated cells)


T(c) cell is stimulated by T(h) cytokines to develop into a CTL, which lyses infected self cells by secreting porforins and cytotoxic enzymes


The specific site on an antigen recognized by an antibody
A low MW substance that combines with a larger molecule to produce an amplified immune reponse
A substance that non-specifically enhances the immune response to antigens, possibly by increasing their uptake by phagocytic cells or promoting time the antigen remains in the body
5 Classes of Antibodies

IgG:Binds 2 antigens; 75% of antibodies

IgE: Binds 2 antigens; major component of the allergic reaction

IgA: Dimerization (J chain); able to bind 4 antigens; takes part in agglutination reaction

IGD:Binds 2 antigens

IGM: Pentamerization (J chain): Able to bind 5 antigens at once


4 mechanisms of antibody action



1) Agglutination: Clumping together of antigens

2) Precipitation: Antigen becomes insoluble

3) Neutralization: Antibody covers the active site

4) Lysis: Antibody bursts infected cell

Functions of the Complement System

1) Amplification of antibody reaction

2) Lysis of foreign cells, bacteria, viruses

3) Opsonization (C3b attached to foreign surface recognized by receptors on phagocytes)

4) Immune Clearance

Classical Pathway

C1q binds to antibody-antigen complex or directly to some pathogen surfaces


C1q binds to 2C1r and 2C1s zymogene


Binding of C1q heads to pathogenic surface initiates C1r enzymatic activity, cleaving of C1s to generate serine protease


Activated C1s cleaves C4 to C4a and

C4b (C4b binds to microbial surface, C4a becomes a chemoattractant)


C4b binds C2, which is cleaved by C1s into C2b and C2a (C2b complexes with C4b to form C3 convertase, C2a becomes a chemoattractant)


C3 convertase cleaves C3 into C3a and C3b (C3b complexes with C3 convertase to form C3/C5 convertase capable of cleaving many C3 to amplify the response, C3a becomes a chemoattractant [inflammatory mediator])


C3/C5 convertase cleaves C5 into C5a (most important chemoattractant and C5b (initiates MAC formation by combining with C6/7/8 and a ring of C9 to create a pore in the cell membrane)


Alternative Pathway

Initiated by spontaneous plasma C3 hydrolysis


C3b is produced at a sig. rate by spontaneous cleavage (C3 tick-over) through spontaneous C3 thioester hydrolysis to form C3(H20), binding factor B. D plasma protease cleaves B to form C3(H2O)Bb (a fluid C3 convertase that cleaves C3 to a and b); most C3b are inactivated by H20

Terminal Complement Components

C5 convertase is formed when a large number of C3b of the pathogen surface bind to C4b2b or C3bBb; C5b initiates assembly of the terminal complement component


Activity: C5a>C3a>C4a


C5a activates mast cells and degranulates mast cell mediators; histamine and TNF-alpha induce inflammation; can also enhance phagocytosis of opsonised microorganisms

Decay-accelerating factor (DAF)
Membrane protein that displaces Bb from C3b and C2b from C4b
Hypersensitivity/Allergic Response

Type 1- IgE mediated (occurs after 2nd exposure; mast cells and basophils release soluble factors) example: latex allergies


Type 2- antibody mediated (antibody destroys cells and platelets by activating the complement system)

example: infusion of an incorrect blood type


Type 3- Immune Complex Mediated (Days-> weeks after original exposure); activates complement system, leads to massive influx of neutrophils

Example: Autoimmune Diseases e.g. diabetes/Lupus


Type 4- Cell mediated; delayed (27-72h post-exposure) response; usu. starts at 2nd exposure; no antibodies; T(h) cells release cytokines that activate macrophages or T(c) cells

Example: response to a metallic biomatl

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