Type II immunopathological reaction

Type II immunopathological reaction. (cytotoxic type) is a humoral reaction, based on IgG and IgM antibodies and subsequent activation of cytotoxic leukocytes by lysis of antibody-labeled cells'''. Importantly, this type of response is elicited by antibodies to antigens located on cell surfaces.'''. The mechanism caused by the gradual activation of complement with the formation of the membranolytic complex of the terminal part of complement (C5b–C9) is also utilized. In some immunopathological conditions, antibodies do not lead to cell death, but to a functional disorder by occupying receptors (followed by receptor stimulation or blockade).

Cytotoxic antibodies
thumb|Krevní skupiny Antibodies of class IgG a IgM have the ability to activate complement and cause antibody dependent cytotoxicity. Phagocytes and NK-cells express Fc-receptors on their surface. These can bind Fc portions of antibody of class IgG. Leukocytes are activated and target cells are killed by cytotoxic mechanisms. At other times, a direct effect on complement activation with the formation of the C5b-C9 membranolytic complex is exerted without cellular involvement.

Transfusion reaction
The reason for this is the existence of antibodies against allelic forms of various surface antigens of red blood cells, platelets and leukocytes. These can occur after the first incorrect transfusion, after a different type of sensibilization etc. Natural IgM and antibodies produced by various microbial polysaccharide antigens (especially intestinal microflora) are found in large amounts in the blood. These IgM antibodeis bind various saccharide structures including those, which are similar to blood group A and B substances. The body does not normally allow the formation of antibodies that react with antigens on the surface of its own cells. In addition to antigens A, B and 0, there are a number of other more or less polymorphic erythrocyte antigens (e.g. Rh system). Repeated transfusion of inappropriate red blood cells can lead to damage mediated by the complement or phagocytes. TThis also applies to neutrophils and platelet alloantigens. Antibodies against allelic forms of Fc-receptors (CD16) of neutrophils are involved in, neonatal neutropenia. Antibodies against platelet aloantigens cause neonatal thrombocytopenia in children of mothers who have given birth several times, které vícekrát rodily, or received blood transfusions.

When blood cells A are transfused into recipient B, antibodies bind and the classical complement pathway is activated. classic complement pathway. This leads to lysis of the „foreing“ cells.
 * Example:

Hemolytic disease of newborns
Is caused by antibodies against  RhD antigens, if the mother RhD- and the fetus is  RhD+ and the mother has been previously immunized against RhD. IgG antibodies cross the placenta and hemolysis of fetal erythrocytes occurs. At the same time neonatal jaundice develops, which can lead to the so-called kernikterus.

Autoimmune diseases
In autoimmune diseases cytotoxic antibodies are used in the so-called. organ specific autoimmune diseases, in which the autoimmune reaction is directed against the autoantigens specific for cell lineage or tissue. Erythrocytes, granulocytes, platelets, membranes of glomeruli, and components of skin are damaged most.

Blocking or stimulating antibodies
A condition in which autoantibodies do not directly destroy the target structure, but block or stimulate its function. Protilátky proti membránovému receptoru mohou stimulovat funkci přirozeného ligandu (tzv. stimulační efekt), nebo naopak soutěžit o vazbu s určitým ligandem a bránit jeho vazbě (blokující efekt). Inhibiční efekt se uplatní nejen u buněk, ale i v případě solubilních proteinů (enzymů). To znamená, že autoprotilátka inhibuje fyziologické funkce příslušného proteinu. Příkladem stimulačních protilátek je Graves-Basedowova choroba proti receptoru TSH (hormon stimulující tyreoideu). Příklad blokujících protilátek je myasthenia gravis. V důsledku vazby autoprotilátky na acetylcholinový receptor je blokován nervosvalový přenos.

Další příklady:
 * protilátky proti vnitřnímu faktoru blokují vstřebávání vitaminu B12 → perniciózní anémie,
 * protilátky proti hormonům štítné žlázy → hypotyreóza,
 * protilátky proti receptoru pro inzulin → formy DM,
 * protilátky proti některým fosfolipidům (kardiolipin) – zasahují do procesu srážení krve → antifosfolipidový syndrom, flebotrombózy,
 * protilátky proti koagulačnímu faktoru VIII → vzácná forma hemofilie,
 * protilátky proti cytoplazmatickým antigenům neutrofilů (ANCA) → patogeneze některých druhů vaskulitid. Ty stimulují oxidační metabolismus granulocytů a inhibují jejich mikrobicidní aktivitu,
 * protilátky proti spermiím, oocytům atd. → poruchy plodnosti.

Související články

 * Alergie
 * Imunopatologická reakce I. typu
 * Imunopatologická reakce III. typu
 * Imunopatologická reakce IV. typu
 * AB0 systém
 * Rh systém

Externí odkazy

 * Imunopatologická reakce II. typu – Youtube video