CD1


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CD1

A family of MHC class I-like molecules expressed on the surface of immature thymocytes, Langerhans cells, and certain B cells; CD1 is a ligand for T cell subpopulation, is present in intestinal epithelium adjacent to GALT, possibly involved in epithelial immunity. See Gut-associated lymphoid tissue.
References in periodicals archive ?
Two-way ANOVA was applied for comparing CD1 and C57BL/6 mice at different time points.
CD1 Mice Display Increased Susceptibility to NTS Compared to C57BL/6 Mice.
Based on these results, 250 [micro]l and 100 [micro]l NTS were selected for subsequent experiments in C57BL/6 and CD1, respectively.
The CD1 NTN mice developed significantly increased UAER on days 2-3, 6-7, and 16-17 compared to C57BL/6 NTN mice (Figure 3(a)).
We previously reported that the CD1 gene is frequently amplified in both the components of esophageal carcinosarcoma.[5,6] As esophageal carcinosarcoma has the same morphologic and immunohistochemical features as carcinosarcoma of the tongue, CD1 gene amplification may be a common important event in the molecular pathogenesis of tumors of this morphologic type.
Recently, Nogueira et al[8] reported that CD1 gene amplification is associated with recurrence and/or metachronous tumors in head and neck squamous cell carcinoma, and Mineta et al[11] reported that CD1 overexpression correlates with poor prognosis in patients with tongue squamous cell carcinoma.
CD1 shares many structural features with MHC class I molecules.
Similarly to MHC class I, CD1 molecules possess two deep pockets: A' and F'.
After translation, CD1 molecules initiate their maturation process in the endoplasmic reticulum (ER).
For immunization C57BL/6 and CD1 mice were injected subcutaneously on day 0 with 200 [micro]L of an emulsion containing 300 [micro]g of [MOG.sub.35-55] (CNB, CSIC, Madrid, Spain) and 800 [micro]g of heat killed Mycobacterium tuberculosis H37RA (Difco, BD Diagnostics, MD) emulsified in incomplete Freund adjuvant oil (Sigma-Aldrich, St.
We explored regulatory and effector immune mechanisms in CD1 and C57BL/6 mice immunized with [MOG.sub.35-55], using as controls nonimmunized mice and mice immunized with [PLP.sub.139-151], a myelin peptide that is not capable of inducing EAE in any of those mouse strains.
Moreover, upon antigen-specific stimulation, the splenocytes from CD1 resistant mice did not proliferate, while those of C57BL/6 susceptible mice did (P = 0.016, Figure 1).