Anti-CD1D (full length) polyclonal antibody

The surface of mammalian bodies is colonized by a multitude of microbial organisms, which under normal conditions support the host and are considered beneficial commensals. This requires, however, that the composition of the commensal microbiota is tightly controlled and regulated. The host immune system plays an important role in the maintenance of this microbiota composition. Here we focus on the contribution of one particular immune cell type, invariant Natural Killer T (iNKT) cells, in this process. The iNKT cells are a unique subset of T cells characterized by two main features. First, they express an invariant T-cell receptor that recognizes glycolipid antigens presented by CD1d, a non-polymorphic major histocompatibility complex class I-like molecule. Second, iNKT cells develop as effector/memory cells and swiftly exert effector functions, like cytokine production and cytotoxicity, after activation. We outline the influence that the mucosal microbiota can have on iNKT cells, and how iNKT cells contribute to the maintenance of the microbiota composition.

Cluster of differentiation (CD)1 molecules are a highly conserved family of MCH-like transmembrane glycoproteins that bind lipid and glycolipid antigens and present a diverse range of microbial and self-glycolipids to antigen-specific T cells. The current study aimed to find out the impact of CD1A and CD1D polymorphisms on pulmonary tuberculosis (PTB). This case-control study encompassed 172 PTB patients and 180 healthy subjects. Genotyping of CD1A and CD1D variants was achieved using the polymerase chain reaction restriction fragment length polymorphism method. The results revealed that CD1A rs411089 variant significantly increased the risk of PTB in recessive model [odds ratio (OR)=2.71, 95% confidence interval (CI)=1.38-5.57, CC vs. TT+TC, P=0.005]. CD1D rs859009 polymorphism significantly reduced the risk of PTB in heterozygous codominant (OR=0.50, 95% CI=0.29-0.86, P=0.011, GC vs. GG) and dominant (OR=0.53, 95% CI=0.31-0.88, P=0.019, GC+CC vs. GG) inheritance model. The CD1A rs366316, CD1D rs973742 and CD1D rs859010 were not associated with the risk/protection from PTB (P>0.05). The results of the present study suggest that CD1A rs411089 and CD1D rs859009 but not CD1A rs366316, CD1D rs973742 and CD1D rs859010 polymorphisms are associated with PTB in a sample of the Iranian population. Further investigation with different ethnicities and larger sample sizes are necessary to certify the findings of the present study.