%0 Journal Article
%A Sevilla Movilla, Silvia
%A Fuentes, Patricia
%A Rodríguez García, Yaiza
%A Arellano Sánchez, Nohemi
%A Krenn, Peter W.
%A Isern de Val, M. Soledad
%A Montero Herradón, Sara
%A Garcia-Ceca Hernández, Javier
%A Burdiel Herencia, Valeria
%A Gardeta, Sofía R.
%A Aguilera Montilla, Noemí
%A Barrio Alonso, Celia
%A Crainiciuc, Georgiana
%A Bouvard, Daniel
%A García-Pardo, Angeles
%A Zapata González, Agustín
%A Hidalgo, Andrés
%A Fässler, Reinhard
%A Carrasco, Yolanda R.
%A Toribio, Maria L.
%A Teixidó, Joaquín
%T ICAP-1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice
%D 2022
%@ 0014-2980; Electronic: 1521-4141
%U https://hdl.handle.net/20.500.14352/72021
%X ICAP-1 regulates β1-integrin activation and cell adhesion. Here, we used ICAP-1-null mice to study ICAP-1 potential involvement during immune cell development and function. Integrin α4β1-dependent adhesion was comparable between ICAP-1-null and control thymocytes, but lack of ICAP-1 caused a defective single-positive (SP) CD8+ cell generation, thus, unveiling an ICAP-1 involvement in SP thymocyte development. ICAP-1 bears a nuclear localization signal and we found it displayed a strong nuclear distribution in thymocytes. Interestingly, there was a direct correlation between the lack of ICAP-1 and reduced levels in SP CD8+ thymocytes of Runx3, a transcription factor required for CD8+ thymocyte generation. In the spleen, ICAP-1 was found evenly distributed between cytoplasm and nuclear fractions, and ICAP-1–/– spleen T and B cells displayed upregulation of α4β1-mediated adhesion, indicating that ICAP-1 negatively controls their attachment. Furthermore, CD3+- and CD19+-selected spleen cells from ICAP-1-null mice showed reduced proliferation in response to T- and B-cell stimuli, respectively. Finally, loss of ICAP-1 caused a remarkable decrease in marginal zone B- cell frequencies and a moderate increase in follicular B cells. Together, these data unravel an ICAP-1 involvement in the generation of SP CD8+ thymocytes and in the control of marginal zone B-cell numbers.
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