Peptidylprolyl isomerase C (Ppic) regulates invariant Natural Killer T cell (iNKT) differentiation in mice. Issue 8 (5th May 2021) - Paiva, Ricardo S.
Abstract: Peptidyl‐prolyl cis‐trans isomerase C ( Ppic ) is expressed in several bone marrow (BM) hematopoietic progenitors and in T‐cell precursors. Since the expression profile of Ppic in the hematoimmune system was suggestive that it could play a role in hematopoiesis and/or T lymphocyte differentiation, we sought to test that hypothesis in vivo. Specifically, we generated a Ppic ‐deficient mouse model by targeting the endogenous locus by CRISPR/Cas9 and tested the requirement of Ppic in hematopoiesis. Several immune cell lineages covering BM progenitors, lymphocyte precursors, as well as mature cells at the periphery were analyzed. While most lineages were unaffected, invariant NKT (iNKT) cells were reduced in percentage and absolute cell numbers in the Ppic ‐deficient thymus. This affected the most mature stages in the thymus, S2 and S3, and the phenotype was maintained at the periphery. Additionally, immature transitional T1 and T2 B lymphocytes were increased in the Ppic ‐deficient spleen, but the phenotype was lost in mature B lymphocytes. In sum, our data show that Ppic is dispensable for myeloid cells, platelets, erythrocytes, αβ, and γδ T lymphocytes in vivo in the steady state, while being involved in B‐ and iNKT cell differentiation. Abstract : Peptidylprolyl isomerase C ( Ppic ) deficient mice were generated and their hematopoietic system analyzed. Loss of Ppic caused a reduction in the number of iNKT cells differentiating in the thymus, which persisted at the periphery. ​