CD44 expressed in the recipient’s tissue rather than on the infiltrating-cells enhances the development of T1D in the cell transfer model.

<p>A) CD44-deficient non-diabetic NOD male recipients were reconstituted with inflammatory spleen cells derived from WT (CD44^+/+→CD44^-/-; marked #1) or CD44-deficient (CD44^-/-→CD44^-/-; marked #2) diabetic NOD female donors. In addition, WT non-diabetic NOD male recipients were reconstituted with inflammatory spleen cells derived from WT (CD44^+/+→CD44^+/+; marked #3) or CD44-deficient (CD44^-/-→CD44^+/+; marked #4) diabetic NOD female donors. Inflammatory cells are marked by arrows and local islet cells by arrowhead. The pancreases of all 4 combinations were removed after detection of diabetes or 200 days after cell transfer. Doing so, pancreases that were harvested approximately at the same time, were stained with anti-CD44 mAb. B) The % of diabetes-free mice (exhibiting less than 250 mg/dL urine glucose) was determined in corresponding four mouse groups, described in <i>A</i>. Statistical analysis by Breslow: #2 versus #3, <i>P</i> < 0.01; #1 versus #2 (follow up 75 to 200 days), <i>P</i> < 0.03; #3 versus #4 (follow up 20 to 75 days), <i>P</i> < 0.03.