CD44-null NOD females display relative resistance to T1D: role of inflammatory cells.

<p>A) and B) Development of T1D in the spontaneous (A) and cell transfer (B) models of WT and CD44-deficient mice was monitored by measuring blood glucose. In the transfer model, irradiated CD44-deficient and WT young (6–8 weeks-old) male recipients were respectively transplanted with splenocytes from CD44-deficient and WT diabetic females. Percentage of diabetes-free mice (showing <250 mg/dL blood glucose) was recorded versus time. Statistical analysis by Breslow; <i>A</i>, <i>P</i> < 0.05; <i>B</i>, <i>P</i> < 0.005. C) The invasion capacity of infiltrating cells derived from WT (n = 6) and CD44-deficient (n = 6) NOD females (spontaneous model) was measured as indicated in <i>Materials and Methods</i>. A total of 754 pancreatic islets in each mouse group were scored by an uninformed observer. The percentage of islets showing each one of the infiltrating scores was calculated for each mouse, and the average values are presented. Islets from CD44-deficient mice display higher percentage of infiltrating scores (2, 3 and 4) than islets from wild type mice. <i>P</i> < 0.0001 by Pearson's χ2 test comparing the distribution of scores in the two mouse groups. D) Wild type or CD44-deficient pre-diabetic spleen cells were added to the top compartment of transwell migration chamber, separated by HA-coated filter (10 μg/filter) from the bottom compartment, and the % of cells migrating through the filter toward the chemoatractant in the bottom compartment was calculated by flow cytometry. Statistical analysis by Student’s-<i>t-</i> test. Accumulated data of 4 experiments (n = 8; error bars, SEM).