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Siddiqui MR Meisner S Tosh K Balakrishnan K Ghei S Fisher SE Golding M Shanker Narayan NP Sitaraman T Sengupta U Pitchappan R Hill AV 《Nature genetics》2001,27(4):439-441
Leprosy, a chronic infectious disease caused by Mycobacterium leprae, is prevalent in India, where about half of the world's estimated 800,000 cases occur. A role for the genetics of the host in variable susceptibility to leprosy has been indicated by familial clustering, twin studies, complex segregation analyses and human leukocyte antigen (HLA) association studies. We report here a genetic linkage scan of the genomes of 224 families from South India, containing 245 independent affected sibpairs with leprosy, mainly of the paucibacillary type. In a two-stage genome screen using 396 microsatellite markers, we found significant linkage (maximum lod score (MLS) = 4.09, P < 2x10-5) on chromosome 10p13 for a series of neighboring microsatellite markers, providing evidence for a major locus for this prevalent infectious disease. Thus, despite the polygenic nature of infectious disease susceptibility, some major, non-HLA-linked loci exist that may be mapped through obtainable numbers of affected sibling pairs. 相似文献
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Kolachala V Asamoah V Wang L Obertone TS Ziegler TR Merlin D Sitaraman SV 《Cellular and molecular life sciences : CMLS》2005,62(22):2647-2657
Adenosine is an endogenous signaling molecule upregulated during inflammatory conditions. Acting through the A2b receptor
(A2bR), the predominant adenosine receptor in human colonic epithelia, adenosine has been directly implicated in immune and
inflammatory responses in the intestine. Little is known about expression and regulation of A2bR during inflammation. Tumor
necrosis factor alpha (TNF-α) is highly upregulated during chronic and acute inflammatory diseases. This study examined the
expression of A2bR during colitis and studied effects of TNF-α on A2bR expression, signaling and function. Results demonstrated
that A2bR expression increases during active colitis. TNF-α pretreatment of intestinal epithelial cells increased A2bR messenger
RNA and protein expression. TNF-α significantly increased adenosine-induced membrane recruitment of A2bR and cyclic adenosine
monophosphate downstream signaling. Further, TNF-α potentiated adenosine-induced shortcircuit current and fibronectin secretion.
In conclusion, we demonstrated that TNF-α is an important regulator of A2bR, and during inflammation, upregulation of TNF-α
may potentiate adenosine-mediated responses.
Received 21 July 2005; received after revision 22 August 2005; accepted 19 September 2005
†These authors contributed equally to this work. 相似文献
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