In type II reactions, the host injury is mediated by antibodies (IgG or rarely IgM) which interact with various types of antigens, such as:

- Host cell surface antigens (e.g. RBC membrane antigens like blood group and Rh antigens)

- Extracellular matrix antigens or

-  Exogenous antigens absorbed on host cells (e.g. a drug coating on RBC membrane).

After Ag-Ab binding occurs, the Fc region of antibody initiates the type II reactions by the following three broad mechanisms (Figs 1A and B).

Fig1A and B: Different mechanisms of antibody mediated type II hypersensitivity reactions: A. Complement-dependent reactions; B. Antibody-dependent cellular cytotoxicity (ADCC).

Abbreviations: RBC, red blood cell; NK, natural killer.

Complement-dependent Reactions

The Fc region of antibody (bound with antigen) can activate the classical pathway of complement system. Activation of classical pathway leads to host cell injury which is mediated by the following three mechanisms (Fig. 1A).

 1. Complement-dependent cytolysis: The membrane attack complex (C5-C9) formed by the activation of classical pathway can produce pores which lead to lysis of the target cells

2. Complement-dependent inflammation: The byproducts of complement pathways such as C3a and C5a are chemoattractants; hence can induce inflammatory response leading to tissue injury

3. Opsonization: By-products of complement pathway, such as C3b and C4b act as opsonins. They deposit on the target cells. Phagocytes, such as macrophage and neutrophil can engulf such C3b and C4b coated target cells via complement receptors.

Antibody-dependent Cellular Cytotoxicity (ADCC)

IgG antibodies can coat on the target cells by interacting with the surface antigens through Fab region. The Fc portion of IgG in turn binds to Fc receptors on various effector cells such as NK cells which result in destruction of the target cells (Fig. 1B).

- ADCC is involved in destruction of the targets that are too large to be phagocytozed, e.g. parasites, tumors or graft rejection

- Although ADCC is typically mediated by IgG antibodies, in certain instances (e.g. eosinophil-mediated killing of parasites) IgE antibodies are used.

Autoantibody Mediated (Antibody-dependent Cellular Dysfunction or ADCD)

 In this condition, the host produces certain autoantibodies which bind and disturb the normal function of human self-antigens.

- Anti-receptor Ab: Antibodies may be directed against human receptors, resulting in either inhibition or excessive activation of the receptors leading to host injury

*  Activation of receptor, e.g. Graves’ disease: Here, the autoantibodies produced are called LATS (long acting thyroid stimulators), which stimulate the thyroid cells to upregulate the production of thyroid hormones

* Inhibition of receptor, e.g. myasthenia gravis: In this condition, anti-acetylcholine (ACh) receptor antibodies are produced; which block the ACh receptors, leading to profound muscular weakness.

- Other examples of ADCD:

* Goodpasture syndrome (antibody produced against type IV collagen)

* Pernicious anemia (antibody directed against intrinsic factor)

* Rheumatic fever (antibody against streptococcal antigens cross reacting with heart)

* Myocarditis in Chagas disease.

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مواضيع ذات صلة

Humoral Immunodeficiency (B Cell Defects)

Type IV Hypersensitivity Reaction

Type III Hypersensitivity Reaction

Detection of Type I Hypersensitivity

Manifestations of Type I Reaction

Mechanism of Type I Hypersensitivity

Self-Recognition (Tolerance)

Hypersensitivity Reactions

Humoral/Antibody-Mediated Immune Response

Cell-Mediated Immune Response

Helper T Cells (Activation AND Differentiation)

Type III (Immune Complex) Reactions