2026-06-27T23:35:04Zhttps://docta.ucm.es/rest/oai/request
oai:docta.ucm.es:20.500.14352/720212023-08-25T16:08:09Zcom_20.500.14352_14col_20.500.14352_15
Docta Complutense author Sevilla Movilla, Silvia author Fuentes, Patricia author Rodríguez García, Yaiza author Arellano Sánchez, Nohemi author Krenn, Peter W. author Isern de Val, M. Soledad author Montero Herradón, Sara author Garcia-Ceca Hernández, Javier author Burdiel Herencia, Valeria author Gardeta, Sofía R. author Aguilera Montilla, Noemí author Barrio Alonso, Celia author Crainiciuc, Georgiana author Bouvard, Daniel author García-Pardo, Angeles author Zapata González, Agustín author Hidalgo, Andrés author Fässler, Reinhard author Carrasco, Yolanda R. author Toribio, Maria L. author Teixidó, Joaquín 2023-06-22T11:01:41Z 2023-06-22T11:01:41Z 2022-05-02 0014-2980; Electronic: 1521-4141 10.1002/eji.202149560 https://hdl.handle.net/20.500.14352/72021 https://doi.org/10.1002/eji.202149560 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. eng Atribución 3.0 España ICAP-1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice journal article URL https://docta.ucm.es/bitstreams/506d668f-3266-46d0-8dba-addfca877581/download File MD5 3e4258fd3a1c49bce33aaf6110f0ebde 5445165 application/pdf Sevilla‐Movilla, S. et al. 2022. ICAP‐1 loss impairs CD8 thymocyte development....pdf