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Nezih Cereb

Publications and source records attributed to Nezih Cereb.

3 recordsLinked to original sources

HLA Diversity of Over 500,000 Individuals on the DATRI Register Across 18 Regions in India.

Registries of unrelated stem cell donors can use HLA haplotype frequencies to aid in registry management. DATRI is India's largest registry with over 550,000 donors, with donors in 35 of India's 36 states and union territories. A geographical based analysis on HLA haplotype frequencies has not previously been carried out with an Indian dataset of this size. To balance granularity and accuracy in estimating 5-locus haplotype frequencies for HLA-A, -C, -B, -DRB1 and -DQB1, we grouped donors into 18 regions with a minimum population size of 2000 donors. We identified the most frequent haplotype as A*33:03-ARD~C*07:01-ARD~B*44:03-ARD~DRB1*07:01-ARD~DQB1*02:01-ARD in Odisha (6.09%), which was also the most frequent haplotype in nine other regions. Assigning the most likely diplotypes to donors, there were a total of 57,959 haplotypes and just 202 (0.3%) of those were present in all 18 regions. HLA-B had the greatest number of alleles across the whole dataset (559) and HLA-DQB1 the least (167). However, HLA-C displayed the most inter-region diversity with only 6.7% of HLA-C alleles present in all regions (average 9.5%). We clustered the regions, using Nei's standard genetic distance, and these correlated with geography; however, three regions (North India, Kerala, and the Gujarat area) did not fit into any cluster. These regions each had one or more distinctive haplotypes that were very frequent (≥ 0.5%) in that region alone. Additionally, the Gujarat area had the lowest diversity metrics. These data can be used to inform the management of registries and contribute to our understanding of HLA diversity globally.

Humans↗

Control of effector CD8+ T cell function by the transcription factor Eomesodermin.

Activated CD8+ T cells play a critical role in host defense against viruses, intracellular microbes, and tumors. It is not clear if a key regulatory transcription factor unites the effector functions of CD8+ T cells. We now show that Eomesodermin (Eomes), a paralogue of T-bet, is induced in effector CD8+ T cells in vitro and in vivo. Ectopic expression of Eomes was sufficient to invoke attributes of effector CD8+ T cells, including interferon-gamma (IFN-gamma), perforin, and granzyme B. Loss-of-function analysis suggests Eomes may also be necessary for full effector differentiation of CD8+ T cells. We suggest that Eomesodermin is likely to complement the actions of T-bet and act as a key regulatory gene in the development of cell-mediated immunity.

Amino Acid Sequence↗

T-bet is a STAT1-induced regulator of IL-12R expression in naïve CD4+ T cells.

T helper type 1 (T(H)1) cell development involves interferon-gamma (IFN-gamma) signaling through signal transducer and activator of transcription 1 (STAT1) and interleukin-12 (IL-12) signaling through STAT4 activation. We examined here T-bet regulation and evaluated the actions of T-bet in STAT1- and STAT4-dependent T(H)1 development processes. We found that T-bet expression during T cell activation was strongly dependent on IFN-gamma signaling and STAT1 activation, but was independent of STAT4. Ectopic T-bet expression strongly increased IFN-gamma production in T(H)2 cells activated by PMA-ionomycin, but weakly increased IFN-gamma production in T(H)2 cells stimulated by IL-12 IL-18 or OVA peptide antigen-presenting cell stimulation. In contrast, IL-12 IL-18 induced IFN-gamma production remained STAT4-dependent despite ectopic T-bet expression. Ectopic T-bet expression selectively induced expression of IL-12Rbeta2, but not IL-18Ralpha, in wild-type and STAT1(-/-) T(H)2 cells, but did not extinguish expression of GATA-3 and T(H)2 cytokines. Finally, ectopic T-bet did not directly induce expression of endogenous T- bet independently of IFN-gamma or STAT1. Thus, T-bet is induced by IFN-gamma and STAT1 signaling during T cell activation. In addition, T-bet mediates STAT1-dependent processes of T(H)1 development, including the induction of IL-12Rbeta2.

Animals↗