Disease relevance of Cd1d1

• We inserted the mouse CD1.1 gene into vaccinia virus to create a recombinant virus expressing CD1.1 under the control of a viral promoter [1].
• CD1 antigen presentation and infectious disease [2].
• CD1d expression on hemopoietic cells promotes CD4+ Th1 response in coxsackievirus B3 induced myocarditis [3].

High impact information on Cd1d1

• The failure to develop AHR can be reversed by the adoptive transfer of tetramer-purified NKT cells producing interleukin (IL)-4 and IL-13 to Ja281(-/-) mice, which lack the invariant T-cell receptor (TCR) of NKT cells, or by the administration to Cd1d(-/-) mice of recombinant IL-13, which directly affects airway smooth muscle cells [4].
• To assess the function of CD1 in lymphocyte development, we generated mice with targeted disruption of the CD1.1 and CD1.2 genes [5].
• CD1.1 is by far the most divergent class I molecule capable of regulating NK cell activity [6].
• The murine nonclassical class I major histocompatibility complex-like CD1.1 molecule protects target cells from lymphokine-activated killer cell cytolysis [6].
• Using this recombinant virus to infect normal or mutant cell lines, we found that the expression of molecules reactive with the CD1.1-specific monoclonal antibody 3C11 requires the expression of beta 2m but was not affected by the absence of the MHC-encoded peptide transporter (TAP) [1].

Biological context of Cd1d1

• The cDNA encoding the murine CD1.1 and CD1.2 gene products were isolated and their complete nucleotide sequence was determined [7].
• The predicted amino acid sequence in the transmembrane region and in the cytoplasmic tail was identical for CD1.1 and CD1 [7].
• Southern blot hybridization of DNA from Chinese hamster x mouse somatic cell hybrids was used to assign the mouse Cd1d genes to chromosome 3 [8].
• Thus, alphaGalCer (which triggers NKT cells and activates NK cells) efficiently increases the resistance to allogeneic bone marrow transplantation while betaGalCer (C12) (which triggers NKT cells but does not activate NK cells) fails to enhance bone marrow graft rejection [9].
• This leaves an important gap in our understanding of the CD1 antigen presentation pathway given the potential role of CD1a, CD1b and CD1c for contributing to antimicrobial immunity [2].

Anatomical context of Cd1d1

• Cell expressing murine CD1.1 were generated after transfer of the CD1.1 cDNA into murine cell lines [7].
• Altogether, the results support the idea that CD1.1 may function in recruiting a form of innate help from specialized cytokine producer alphabeta T cells to APCs, a role that might be important at the preadaptive phase of immune responses to some microbial pathogens [10].
• CD1.1 expression by mouse antigen-presenting cells and marginal zone B cells [10].
• Its recognition by a panel of 12 V alpha14-positive and -negative CD1-specific alphabeta T cell hybridomas was blocked by two groups of mAbs that bound to adjacent clusters of epitopes, indicating that different alphabeta TCRs bind to the same region of CD1.1, presumably above the groove [10].
• Remarkably, CD1.1 was mainly expressed by dendritic cells, B cells, and macrophages, suggesting a function in Ag presentation to Th cells [10].

Associations of Cd1d1 with chemical compounds

• We have now discovered another ceramide compound, beta-galactosylceramide (betaGalCer) (C12), that efficiently diminishes the number of detectable mouse NKT cells in vivo without inducing significant cytokine expression or activation of NK cells [9].

Other interactions of Cd1d1

• CD1.1 is a heavily glycosylated, beta2-microglobulin-associated surface protein [10].
• These results show that different CD1.1 self Ags are expressed in different tissues and can be specifically recognized by autoreactive T cells [11].

Analytical, diagnostic and therapeutic context of Cd1d1

• Results of the sequence analysis of genomic DNA from developing DN32H6 beta Tg thymocytes revealed that the frequency of the parental alpha-chain sequence, in this instance the Valpha14-Jalpha281 canonical alpha-chain, is specifically and in a CD1.1-dependent manner, increased in the postselection thymocyte population [12].
• Co-culture of enriched CD4+ cells from infected CD1d-/- and BALB/c mice with Vgamma4+ T cells demonstrated that the Vgamma4+ cells bias the CD4+ cell response to the Th1 phenotype through CD1d [3].

References