On a key postulate of T-cell receptor restrictive function: the V-gene loci act as a single pool encoding recognition of the polymorphic alleles of the species major histocompatibility complex

The proposition that single Valpha or Vbeta gene segments specify the recognition of the allele-specific determinants expressed on the major histocompatibility complex-encoded restricting elements of the species has as its consequence a totally different picture of the functioning of the T-cell receptor. This commentary justifies this assumption and outlines some of its most important consequences.     

A monoclonal antibody to a determinant of the rat T cell antigen receptor expressed by a minor subset of T cells

A hybridoma producing the monoclonal antibody HIS42 was isolatedfrom a fusion between spleen cells from a BALB/c mouse immunizedwith rat thymocytes and the fusion partner SP2/0. This antibodyrecognizes a minor subset of T cells in every haplotype of rattested so tar. The subpopulation of HIS42 positive T cells containsboth CD4+ and CD8+ cells, in the same ratio as found in theperipheral T cell population. When bound to Sepharose beads,HIS42 induces T cell proliteration in the presence of Interleukin-2.In contrast to lymph node T cells, a number of thymocytes werefound to express HIS42 only in the cytoplasm or together withmembrane expression. Most bright HIS42 surface labelled thymocyteswere also positive for MRC OX-44, a marker predominantly identifyingmature thymocytes. SDS-PAGE analyses of the membrane moleculeslmmunoprecipitated by HIS42 show two bands on unreduced gels.One of these bands (85 kd) runs as two separate bands at 35and 48 kd on reduction. The other much weaker broad band ({smalltilde}100 kd) is hardly affected by reduced conditions. Takentogether these data suggest that HIS42 is directed against adeterminant on the rat T cell receptor for antigen, which iscommon to a small number of T cells.     

Insight into the role of TSLP in inflammatory bowel diseases

Proinflammatory cytokines are thought to modulate pathogeneses of various inflammatory bowel diseases (IBDs). Thymic stromal lymphopoietin (TSLP), which has been studied in various allergic diseases such as asthma, atopic dermatitis (AD) and eosinophilic esophagitis (EoE), has been less considered to be involved in IBDs. However, mucosal dendritic cells (DCs) induced by various cytokines including TSLP were reported to cause polarization of T cell toward Th2 response, the differentiation of regulatory T-cell (Treg), and secretion of IgA by B cells. In this review, we discuss the concept that decreased TSLP has the potential to accelerate the development of Th1 response dominant diseases such as the Crohn's disease (CD) while increased TSLP has the potential to lead to a development of Th2 cell dominant diseases such the ulcerative colitis (UC). To examine TSLP's role as a potential determining factor for differentiating UC and CD, we analyzed the effects of other genes regulated by TSLP in regards to the UC and CD pathogeneses using data from online open access resources such as NetPath, GeneMania, and the String database. Our findings indicate that TSLP is a key mediator in the pathogenesis of IBDs and that further studies are needed to evaluate its role.