B cell dynamics



Yolanda R. Carrasco

Group Leader



Research summary

B cells are essential effectors of the adaptive immune response to pathogens. They are responsible for pathogen neutralization and clearance through the production of antigen-specific antibodies. The prompt onset of the humoral immune response is thus crucial in the fight against invaders. This process depends critically on the ability of naïve B cells to search for antigen in secondary lymphoid organs.



Andrada E, Almena M, de Guinoa JS, Merino-Cortes SV, Liébana R, Arcos R, Carrasco S, Carrasco YR, Merida I. Diacylglycerol kinase ζ limits the polarized recruitment of diacylglycerol-enriched organelles to the immune synapse in T cells. Science Signaling, 2016 Dec 20; 9 (459):ra127.

Robles EF, Mena-Varas M, Barrio L, Merino-Cortés SV, et al. Homeobox NKX2-3 promotes marginal-zone lymphomagenesis by activating B-cell receptor signalling and shaping lymphocyte dynamics. Nature Communications, 2016; 7: 11889.

Barrio L, Delgado Cuevas V, Menta R, Mancheño-Corvo P, delaRosa O, Dalemans W, Lombardo E, Carrasco YR. Human adipose tissue-derived mesenchymal stem cells promote B cell motility and chemoattraction. Cytotherapy 2014; 16:1692-1699

Barrio L, Saez de Guinoa J, Carrasco YR. TLR4 shapes B cell dynamics via MyD88-dependent pathways and Rac GTPases. J Immunol 2013; 191:3867-3875

Sáez de Guinoa J, Barrio L, Carrasco YR. Vinculin arrests motile B cells by stabilizing integrin clustering at the immune synapse. J Immunol 2013; 191:2742-2751



Lymphocytes travel across tissue barriers and move through the interstitial space in response to external signals. Continuous migration allows them to seek for pathogen-derived antigens at secondary lymphoid organs, moving throughout the stromal cell network. Antigen recognition halts motile lymphocytes and leads to the Immune Synapse (IS) formation with the antigen-presenting cell; this long-lasting cell-to-cell interaction is critical for lymphocyte activation. Lymphocytes are also exposed to a variety of non-cognate signals such as innate/inflammatory stimuli that modify cell motility/adhesion abilities and cell localization. Lymphocyte dynamics plasticity is thus intrinsic to lymphocyte function and crucial for adaptive immune protection. The knowledge of the molecular mechanisms that govern lymphocyte behaviour will reveal essential aspects of the immune response with potential therapeutic application.

We investigate how distinct stimuli (chemokines, antigen, innate signals) shape B lymphocyte dynamics to regulate cell function. We identified the molecular axis Syk/PIP2/Vinculin as a major regulator of  B cell motility and stable adhesion in response to chemokine and antigen. We are currently studing two proteins implicated in this axis: Bruton´s Tyrosine kinase (Btk) and Diacylglycerol kinase (DGK). Btk is a target of Syk, and its kinase activity promotes the calcium influx while, through its scaffold activity, Btk brings PIP5KI to the plasma membrane to produce PIP2. Btk disfunction causes X-linked immunodeficiencies; Btk targeting with pharmacological inhibitors has very good results in patients with B cell-related lymphoproliferative disorders. DGK consumes DAG to produce phospatidic acid (PA); PA is an allosteric modulator of PIP5KI and a regulator of DOCK2/Rac/F-actin axis. We extend our research to the changes in cell behaviour associated with lymphomagenesis. Our results in a marginal-zone lymphoma mouse model showed that cell dynamics alterations in the whole polyclonal B cell population preceded monoclonal B cell transformation and tumourogenesis.





Yolanda R Carrasco Principal investigator
Sara Violeta Merino Cortés Predoctoral scientist
Sara Román García Predoctoral scientist

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