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Untitled - D Ank Unlimited

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macrophage inflammatory protein 1β(MIP-1β) 475 macrophage migration inhibitory factor<br />

MIP-1α (NMR).<br />

Macrophage inflammatory protein 1α.<br />

endotoxin may secrete this protein, termed MIP-1, which<br />

differs from tumor necrosis factor (TNF), interleukin-1<br />

(IL1), and other endogenous pyrogens because its action<br />

is not associated with prostaglandin synthesis. It appears<br />

indistinguishable from hematopoietic stem cell inhibitor<br />

and may function in growth regulation of hematopoietic<br />

cells. It has a broad spectrum of biological activities<br />

that include prostaglandin-independent pyrogenic activity,<br />

possible participation in wound healing, monocyte<br />

chemotaxis, and suppression of immature bone marrow<br />

Normal<br />

cells<br />

Ovalbumin–<br />

sensitive<br />

cells<br />

Toxoid–<br />

sensitive<br />

cells<br />

COOH<br />

stem and progenitor cells. Significantly, MIP-1α has an<br />

HIV-suppressive effect. Tissue sources include fibroblasts,<br />

monocytes, lymphocytes, neutrophils, eosinophils, smooth<br />

muscle cells, mast cells, platelets, and bone marrow stromal<br />

cells, among other cell types. T lymphocytes, basophils,<br />

hematopoietic precursor cells, monocytes, eosinophils, neutrophils,<br />

mast cells, natural killer (NK) cells, and dendritic<br />

cells, among other types, are target cells.<br />

macrophage inflammatory protein 1(MIP-1)<br />

A chemokine of the β (CC) family. It shares 70% homology<br />

with MIP-1α. Although the two molecules resemble<br />

one another structurally, they are significantly different in<br />

functions. Unlike MIP-1α, MIP-1β does not activate neutrophils.<br />

Unlike MIP-1α, which inhibits early hematopoietic<br />

progenitor growth, MIP-1β potentiates it. Both MIP-1α<br />

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

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

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

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

lymphocytes, hematopoietic precursor cells and basophils<br />

are target cells.<br />

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

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

comprised of MIP-2α, also called 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.<br />

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

antibody effectively decreases neutrophil influx and PAS<br />

positive deposits containing fibrin. Tissue sources include<br />

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

macrophages, epidermal cells, and nasal and bronchial<br />

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

the target cells.<br />

macrophage migration inhibitory factor<br />

Migration inhibitory factor.<br />

No antigen Ovalbumin Toxoid<br />

A B<br />

D<br />

G<br />

E F<br />

H I<br />

Macrophage migration test.<br />

C<br />

M

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