Microbiology & Immunology - Research Publications

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Author: Berzins, Stuart × Author: Godfrey, Dale × Author: Pellicci, Daniel × End date: 2009 × Start date: 2000 ×

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    Localization of Idd11 is not associated with thymus and NKT cell abnormalities in NOD mice
    Brodnicki, TC ; Fletcher, AL ; Pellicci, DG ; Berzins, SP ; McClive, P ; Quirk, F ; Webster, KE ; Scott, HS ; Boyd, RL ; Godfrey, DI ; Morahan, G (AMER DIABETES ASSOC, 2005-12)
    Congenic mouse strains provide a unique resource for genetic dissection and biological characterization of chromosomal regions associated with diabetes progression in the nonobese diabetic (NOD) mouse. Idd11, a mouse diabetes susceptibility locus, was previously localized to a region on chromosome 4. Comparison of a panel of subcongenic NOD mouse strains with different intervals derived from the nondiabetic C57BL/6 (B6) strain now maps Idd11 to an approximately 8-Mb interval. B6-derived intervals protected congenic NOD mice from diabetes onset, even though lymphocytic infiltration of pancreatic islets was similar to that found in NOD mice. In addition, neither thymic structural irregularities nor NKT cell deficiencies were ameliorated in diabetes-resistant congenic NOD mice, indicating that Idd11 does not contribute to these abnormalities, which do not need to be corrected to prevent disease.
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    The influence of CD1d in postselection NKT cell maturation and homeostasis
    McNab, FW ; Berzins, SP ; Pellicci, DG ; Kyparissoudis, K ; Field, K ; Smyth, MJ ; Godfrey, DI (AMER ASSOC IMMUNOLOGISTS, 2005-09-15)
    After being positively selected on CD1d-expressing thymocytes, NKT cells undergo a series of developmental changes that can take place inside or outside the thymus. We asked whether CD1d continues to play a role in late-stage NKT cell development and, in particular, during the functionally significant acquisition of NK1.1 that is indicative of NKT cell maturity. We report that CD1d is indeed crucial for this step, because immature NK1.1(-) NKT cells fail to fully mature when transferred to a CD1d-deficient environment. Surprisingly, however, the lack of CD1d did not greatly affect the long-term survival of NKT cells, and they continued to express CD69 and slowly proliferate. This directly contradicts the currently held view that these phenomena are caused by autoreactivity directed against CD1d/TCR-restricted self-Ags. Our findings demonstrate an ongoing role for TCR-mediated signaling throughout NKT cell development, but the characteristic semiactivated basal state of NKT cells is controlled by CD1d-independent factors or is intrinsic to the cells themselves.