T

Complement adivalion, binding or phagocytes Is opsonized eel v a C3b and Fe receptors

Fe recsplor

C1 hirei.-Kj to Ig

Complement adivalion, binding or phagocytes Is opsonized eel v a C3b and Fe receptors

Fe recsplor

C1 hirei.-Kj to Ig

C3b rOcGptor

(D) A-^ibwiy-dipcndenicciiuiiireyiijtHjKicityiAOCC)

C3b rOcGptor

Rieoqfiiliori by PfK as

Rieoqfiiliori by PfK as

Nalural Kaller INK) cell

Fc ifreiplor '

Nalural Kaller INK) cell

Phagocyte

Phaqocylosis

Phaqocylosis

Phagocytosed cell

Phagocytosed cell

Tüigil c*B lysis

Figure 3 Effector mechanisms in antibody-mediated cell injury. (A) Activation of complement and cell lysis. (B) Activation of complement and recruitment/activation of leukocytes leading to cell lysis. (C) Phagocytosis of opsonized cells. (D) Cell lysis by natural killer cells. (Reproduced with permission from Abbas et al (1994).)

test in which the autoimmune reaction is detected by an agglutination obtained with the addition of human-specific immunoglobulin which agglutinates the autoantibody-coated cells.

Finally, in certain autoimmune diseases, type II reactions can cause immunopathologic damage as the autoantibodies are directed to cell surface or to cytoplasmic antigens. Goodpastures syndrome, pemphigus and myasthenia gravis are all caused by auto antibodies directed to cell surfaces antigens. In Goodpastures syndrome the autoantibodies are directed to the glomerular basement membrane, causing glomerulonephritis, and sometimes also to the alveolar basal membrane, causing lung hemorrhage. In pemphigus the pathogenetic antibodies are directed to desmosome antigens and cause the breakdown of the epidermis. In myasthenia gravis the autoimmune destruction is directed against acethyl-

coline receptors and is responsible for extreme muscular weakness. Conversely, in other organ-specific autoimmune diseases, such as insulin-dependent diabetes mellitus (IDDM) and Hashimotos thyroiditis, the autoantibodies are mainly directed against cytoplasmic antigens (islet cells and thyroid peroxidase, respectively). Their pathogenic relevance is still uncertain. There are indications that IDDM and Hashimotos disease might be caused by a T rather than B cell mediated mechanism.

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