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MIP-2 (macrophage inflammatory protein 2) 498 mitochondrial autoantibodies (MAs)<br />

MIP-1β exert synergistic HIV-suppressive effects. Tissue<br />

sources include monocytes, fibroblasts, T lymphocytes, B<br />

lymphocytes, neutrophils, smooth muscle cells, mast cells,<br />

and selected tumor cell lines. Monocytes, T lymphocytes,<br />

hematopoietic precursor cells, and basophils are target cells.<br />

MIP-2 (macrophage inflammatory protein 2)<br />

A chemokine of the α (CXC) family. The MIP-2 class is<br />

comprised of MIP-2α, also termed GRO-β gene product,<br />

and MIP-2β, the GRO-γ gene product. MIP-2 has a role in<br />

anti-GBM antibody-induced glomerulonephritis in mice. Anti-<br />

MIP-2 antibody injection 30 minutes before anti-GBM antibody<br />

effectively decreases neutrophil influx and PAS-positive<br />

deposits containing fibrin. Tissue sources include mast cells,<br />

cardiac myocytes, mesangial cells, alveolar macrophages,<br />

epidermal cells, human nasal, and bronchial epithelium.<br />

Neutrophils, basophils, and epithelial cells are the target cells.<br />

MIRL (membrane inhibitor of reactive lysis)<br />

Inhibitor of membrane attack complexes on self tissue. Also<br />

known as CD59.<br />

missing self hypothesis<br />

The hypothesis that interaction of NK cells with cells failing<br />

to express self MHC class I antigens on their surfaces<br />

leads to T cell activation. Examples include neoplastic cells;<br />

virus-infected cells; and allogeneic cells.<br />

N.A. Mitcheson.<br />

Mitcheson, N.A. (1928–)<br />

British investigator who demonstrated the role of helper T<br />

cells in immunoregulation.<br />

mitochondria<br />

Cytoplasmic organelles in aerobic eukaryotic cells where<br />

respiration, electron transport, oxidative phosphorylation,<br />

and citric acid cycle reactions occur. Mitochondria possess<br />

DNA and ribosomes.<br />

mitochondrial antibodies<br />

Immunoglobulin G (IgG) antibodies present in 90 to 95% of<br />

primary biliary cirrhosis (PBC) patients. These antibodies,<br />

which are of doubtful pathogenic significance, are specific<br />

for the pyruvate dehydrogenase enzyme complex E2<br />

component situated at the inner mitochondrial membrane<br />

(M2). They are also specific for another E2-associated<br />

protein. Other antimitochondrial antibodies include the M1<br />

Mitochondrial autoantibodies.<br />

Mitochondrial antibody (mouse kidney, 500× magnification).<br />

Mitochondrial autoantibodies (mouse kidney and stomach).<br />

antibodies of syphilis, the M3 antibodies found in pseudolupus,<br />

the M5 antibodies in collagen diseases, the M6 antibodies<br />

in hepatitis induced by iproniazid, the M7 antibodies<br />

associated with myocarditis and cardiomyopathy, the M8<br />

antibodies that may be markers for prognosis, and the M9<br />

antibodies that serve as markers for beginning primary<br />

biliary cirrhosis. Mitochondrial antibody titer may be an<br />

indicator of primary biliary cirrhosis progression. A patient<br />

with a titer of 1 to 40 or more should be suspected of having<br />

primary biliary cirrhosis, whether symptoms are present or<br />

absent and even if alkaline phosphatase is normal.<br />

mitochondrial autoantibodies (MAs)<br />

Immunoglobulin G (IgG) autoantibodies specific for the<br />

E2 component (lipoate acetytransferase) of the pyruvate<br />

dehydrogenase enzyme complex located at the inner

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