B cell immunobiology
B lymphocytes are the only cell type in the organism capable of producing antibodies (Abs), which play an essential role in controlling replication of many pathogens. B cells may have a pathogenic role if they generate antibodies against the self-antigens, called autoantibodies.
B lymphocytes after stimulation, in particular contexts, can differentiate into short- or long-lived plasma cells or memory B cells. The latter cells are part of immunologic memory and responsible for lasting humoral immunity. In addition, B lymphocytes can influence immunity in multiple ways such as antigen presentation to T cells, expression of surface co-stimulatory/inhibitory molecules and cytokine secretion. Consequently, B cells can act as drivers of innate and adaptive immunity.
Our research group is dedicated to the study of the signals that control B lymphocytes survival and differentiation into Plasma cells and regulatory B lymphocytes (Bregs) and their role in infections and autoimmunity.
Specifically, the projects currently underway are focus on the:
- Role of plasma cells in the regulation of inflammation in Trypanosoma cruzi infection
- Role of B cells in the induction of specific CD8+ T cells in Trypanosoma cruzi infection
- Role of Galectin-3 in the generation of Germinal Centers and long-lived plasma cells
- Identification of B cells and immune mediators to establish diagnosis, clinical course and appropriate treatments in patients with Rheumatoid Arthritis
In all the research labor, we work closely together with Drs. Eva Acosta Rodriguez and Carolina Montes and their groups.
The regulatory role of B cells in autoimmunity, infections and cancer: perspectives beyond IL10 production. Gorosito Serran M, Fiocca Vernengo F, Beccaria C, Acosta Rodriguez EV, Montes CL, Gruppi A. FEBS Lett. 2015 Sep 28. pii: S0014-5793(15)00834-0.
Trypanosoma cruzi trans-sialidase initiates an ROR-gt/AHR independent program leading to IL-17 production by activated B cells. Daniela A Bermejo, Shaun W Jackson, Melisa Gorosito-Serran, Eva V Acosta-Rodriguez, Maria C Amezcua-Vesely, Blythe D Sather, Akhilesh K. Singh, Socheath Khim, Juan Mucci, Denny Liggitt, Oscar Campetella, Mohamed Oukka, Adriana Gruppi, David J Rawlings. Nature Immunology. 2013 May:14(5):415-522. FI 24,973
FcgammaRIIb and BAFF differentially regulate peritoneal B1 cell survival. MC Amezcua Vesely, M Schwartz, DA Bermejo, CL Montes, A Kalergis, D Rawlings, EV Acosta-Rodríguez, A Gruppi. Journal of Immunolology. 2012 May 15;188(10):4792-800. Epub 2012 Apr 18. FI: 5,745.
Trypanosoma cruzi infection induces a massive extrafollicular and follicular splenic B cell response which is a high source of non-parasite specific antibodies. DA Bermejo, MC Amezcua-Vesely, M Kahn, EV Acosta-Rodríguez, CL Montes, MC Merino, KM Toellner, E Mohr, D Taylor, A Cunningham, A Gruppi. Immunology 2011 Jan;132(1):123-33. FI:3,432
BAFF mediates splenic B cell response and antibody production in experimental Chagas disease. DA Bermejo, MC Amezcua-Vesely, CL Montes, MC Merino, H Cejas, EV Acosta-Rodríguez, A Gruppi. PLOS Neglected Tropical Diseases. 2010 May 4;4(5):e679. FI:4,172
Cytokines and chemokines shaping the B-cell compartment. EV Acosta-Rodriguez, MC Merino, CL Montes, CC Motrán and A Gruppi. Cytokine and Growth Factor Reviews. 2007. Feb-Apr;18(1-2):73-83.
BAFF and LPS cooperate to induce B cells to become susceptible to CD95/Fas-mediated cell death. EV Acosta-Rodríguez, A Craxton, DW Hendricks, MC Merino, CL Montes, EA Clark and A Gruppi. European Journal of Immunology. 2007. Apr;37(4):990-1000.
Depletion of immature B cells during Trypanosoma cruzi infection: involvement of myeloid cells and cyclooxigenase pathway. E. Zúñiga, EV Acosta-Rodríguez, MC Merino, CL Montes and A Gruppi. European Journal of Immunology. 2005. Jun;35(6):1849-58.
Galectin-3 Mediates Interleukin-4-Induced Survival and Differentiation of B Cells. Functional Cross-talk and Implications during Trypanosoma cruzi Infection. EV Acosta-Rodríguez, E Zúñiga, CL Montes, CC Motrán, FT Liu, GA Rabinovich y A Gruppi. Journal of Immunology. 2004. Jan 1;172(1):493-502.
Trypanosoma cruzi infection selectively renders parasite-specific IgG+ B lymphocytes susceptible to Fas/ Fas ligand-mediated fratricide. E Zúniga, C Motrán, C Montes, H Yagita and A Gruppi. Journal of Immunology 168 (8): 3965 – 73. 2002.