Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cloned cell line was established from tumor cells spontaneously developed in a coculture of an autoreactive T cell line (1/+ T1) and 30 Gy-irradiated MRL/+ spleen cells with Con A supernatants. Morphological studies and studies of histamine content and modes of histamine release after stimulation with compound 48/80 revealed that the cell line (MRL-MC3) had mast cell characteristics. MRL-MC3 was transplantable not only to MRL/+, MRL/lpr and AKR/J (H-2k) mice but also to BALB/c and (BALB/c x DBA/2) F1 (H-2d) mice, although the allogeneic mice survived twice as long as syngeneic mice after i.v. injection. In addition, after i.v. injection, the mast cells infiltrated the livers and spleens of syngeneic (MRL/+) mice, however the lymph nodes around the mesenterium to the parapylorus in allogeneic (BALB/c) mice. A mast cell line (BALB-MC) was also established from a lymph node of MRL-MC3-injected BALB/c mice. Cell surface marker analyses revealed clear differences between the BALB-MC and the original MRL-MC3, which was positive for the expression of MHC class I antigens (K, D), I-E antigen and c-abl-encoded (anti-pEX-2 antibody-reactive) proteins, but not for I-A on the cell surface. In contrast, BALB-MC showed positive only for the MHC class I antigens (K, D) on the surface, and also positive for anti-pEX-2 antibody-reactive cytoplasmic proteins, as seen in MRL-MC3. Mast cells obtained from MRL-MC3-injected MRL/+ mice showed the same staining pattern as MRL-MC3. BALB-MC induced shorter survival times (approximately half) in both MRL/+ and BALB/c mice than MRL-MC3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Transplantability and MHC antigen expression of tumor mast cells. 846 97

The MHC class I-specific inhibitory receptors on human and mouse NK cells have surprisingly different structures. The mouse receptors (Ly-49) are type II transmembrane glycoproteins of the C-type lectin family, whereas the human receptors (killer cell inhibitory receptors (KIR)) belong to the Ig superfamily. This difference prompted a search for Ig-like inhibitory receptors in mice. Here we show that gp49, a mouse mast cell protein of unknown function but with sequence similarity to KIR, is expressed in NK cells. The gp49 cytoplasmic tail, containing a sequence related to an inhibitory motif shared by KIR and Ly-49, delivered a strong inhibitory signal in both human and mouse NK cells when substituted for a KIR cytoplasmic tail. These data show that Ig-like receptors with inhibitory properties exist in both species and that mouse mast and NK cells may recognize common inhibitory ligands.
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PMID:Type I transmembrane receptor with inhibitory function in mouse mast cells and NK cells. 897 69

CD8, a marker largely restricted to subsets of T lymphocytes and NK cells, was detected on freshly isolated rat peritoneal mast cells (PMC). Using flow cytometry, Percoll-enriched rat PMC (> or = 98% purity) were positive for the hinge region of CD8alpha (67.5 +/- 9.5%; Ab OX8) and CD8beta (27.8 +/- 2.3%; Ab 341). CD8+ PMC consisted of two populations, CD8alpha+ (22.5%) and CD8alpha+ beta+ (15.9%). Interestingly, G28, an Ab that identifies the IgV-like region of CD8alpha on T lymphocytes, did not bind PMC, suggesting that PMC CD8alpha is distinct from that on T lymphocytes. Moreover, a similar pattern of Ab positivity for CD8 was observed on a rat mast cell line, RBL 2H3. The presence of CD8alpha immunoreactivity on rat PMC was further confirmed by confocal microscopy. In situ reverse-transcription PCR and reverse-transcription PCR analysis demonstrated that PMC contained mRNA transcripts encoding CD8alpha. In functional studies of CD8 on PMC, both TNF-alpha and nitric oxide production were induced by OX8 (CD8alpha) and 341 Ab (CD8beta) in a dose-dependent manner. However, neither OX8 nor 341 induced histamine secretion from PMC. Ag-induced secretion of TNF-alpha, nitric oxide, and histamine was not affected by OX8 or 341 Abs, suggesting that there are distinct signaling mechanisms mediated by CD8 and Fc epsilonRI. These results indicate that rat PMC express functional CD8 molecules that may be distinct from those of T lymphocytes. The difference suggests there is a ligand other than MHC class I for mast cell CD8.
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PMID:Mast cells express novel CD8 molecules that selectively modulate mediator secretion. 983 15

Killer cell inhibitory receptors (KIRs) inhibit NK and T cell cytotoxicity when recognizing MHC class I molecules on target cells. They possess two tandem intracytoplasmic immunoreceptor tyrosine-based inhibition motifs (ITIMs) that, when phosphorylated, each bind to the two Src homology 2 domain-bearing protein tyrosine phosphatases SHP-1 and SHP-2 in vitro. Using chimeric receptors having an intact intracytoplasmic KIR domain bearing both ITIMs (N + C-KIR), a deleted domain containing the N-terminal ITIM only (N-KIR), or a deleted domain containing the C-terminal ITIM only (C-KIR), we examined the respective contributions of the two ITIMs in the inhibition of cell activation in two experimental models (a rat mast cell and a mouse B cell line) that have been widely used to analyze KIR functions. We found that the two KIR ITIMs play distinct roles. When coaggregated with immunoreceptor tyrosine-based activation motif-bearing receptors such as high-affinity IgE receptors or B cell receptors, the N + C-KIR and the N-KIR chimeras, but not the C-KIR chimera, inhibited mast cell and B cell activation, became tyrosyl-phosphorylated, and recruited phosphatases in vivo. The N + C-KIR chimera recruited SHP-1 as expected, but also SHP-2. Surprisingly, the N-KIR chimera failed to recruit SHP-1; however, it did recruit SHP-2. Consequently, the N-terminal ITIM is sufficient to recruit SHP-2 and to inhibit cell activation, whereas the N-terminal and the C-terminal ITIMs are both necessary to recruit SHP-1. The two KIR ITIMs, therefore, are neither mandatory for inhibition nor redundant. Rather than simply amplifying inhibitory signals, they differentially contribute to the recruitment of distinct phosphatases that may cooperate to inhibit cell activation.
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PMID:Differential roles of N- and C-terminal immunoreceptor tyrosine-based inhibition motifs during inhibition of cell activation by killer cell inhibitory receptors. 1009 67

In addition to being a major effector cell in the elicitation of allergic inflammation, mast cells have been found to be activated in various T cell-mediated inflammatory processes and to reside in close physical proximity to T cells. Such observations and the wide spectrum of mediators produced and secreted by mast cells have led investigators to propose a functional relationship between these 2 cell populations. Indeed, mast cell activation has been reported to induce T-cell migration either directly by the release of chemotactic factors, such as lymphotactin or IL-16, or indirectly by the induction of adhesion molecule expression on endothelial cells. Mast cells are also able to present antigens to T cells, resulting in their activation in either an MHC class I- or class II-restricted and costimulatory molecule-dependent fashion. Adhesion molecule-dependent intercellular contact or MHC class II cognate interactions between T cells and mast cells result in the release of both granule-associated mediators and cytokines from the latter. Also, T cell-derived mediators, such as beta-chemokines, directly induce mast cell degranulation. On the other hand, mast cell-derived cytokines, such as IL-4, have been found to polarize T cells to preferentially differentiate into the T(H2) subset. Thus T cell-mast cell interactions are bidirectional, fulfilling regulatory and/or modulatory roles affecting various aspects of the immune response.
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PMID:Mast cell-T cell interactions. 1048 20

In the last years there has been a growing number of reports concerning the role of mast cells in host defense against bacteria. The mast cell membrane is replete with many receptors/molecules, including those that promote the recognition and binding of bacteria. Mast cells exhibit two basic mechanisms of microbial recognition: opsonin-dependent (via Fc and C3 receptors) and opsonin-independent (via integrins, CD48 molecule and Toll-like receptors). Moreover, mast cells phagocytose and kill adherent bacteria. Phagocytosis of bacteria results in the presentation of bacterial antigens for MHC class I to T cells.
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PMID:[The mast cells phagocytose bacteria]. 1555 77

Stress alters murine hair growth, depending on substance P-mediated neurogenic inflammation and nerve growth factor (NGF), a key modulator of hair growth termination (catagen induction). Whether this is of any relevance in human hair follicles (HFs) is completely unclear. Therefore, we have investigated the effects of substance P, the central cutaneous prototypic stress-associated neuropeptide, on normal, growing human scalp HFs in organ culture. We show that these prominently expressed substance P receptor (NK1) at the gene and protein level. Organ-cultured HFs responded to substance P by premature catagen development, down-regulation of NK1, and up-regulation of neutral endopeptidase (degrades substance P). This was accompanied by mast cell degranulation in the HF connective tissue sheath, indicating neurogenic inflammation. Substance P down-regulated immunoreactivity for the growth-promoting NGF receptor (TrkA), whereas it up-regulated NGF and its apoptosis- and catagen-promoting receptor (p75NTR). In addition, MHC class I and beta2-microglobulin immunoreactivity were up-regulated and detected ectopically, indicating collapse of the HF immune privilege. In conclusion, we present a simplistic, but instructive, organ culture assay to demonstrate sensitivity of the human HF to key skin stress mediators. The data obtained therewith allow one to sketch the first evidence-based biological explanation for how stress may trigger or aggravate telogen effluvium and alopecia areata.
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PMID:Probing the effects of stress mediators on the human hair follicle: substance P holds central position. 1805 48