B cell immunobiology

Work team
Work team
Work team

Research Project

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 antibody-secreting cells and into regulatory B lymphocytes (Bregs) and their role in infections and autoimmunity.

Specifically, the projects currently underway are focus on the:

  • Role of extrafollicular plasmablast in the regulation of inflammation and humoral immune response in Trypanosoma cruzi infection.
  • Identification of cells and soluble mediators involved in the induction and survival of germinal centers, key structures in the generation of high affinity antibodies.
  • Identification of Breg, Tfh and Tfr characteristics 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.

Selected publications

Clinic Immunology

Inhibitory receptor expression on T cells as marker of disease activity and target to regulate effector cellular responses in Rheumatoid Arthritis. Onofrio, Luisina; Zacca, Estefania; Ferrero, Paola; Acosta, Cristina; Mussano, Eduardo; Onetti, Laura; Cadile, Isaac; Gazzoni, Maria; Jurado, Raul; Tosello Boari, Jimena; Ramello, Maria; Montes, Carolina; Gruppi, Adriana; Acosta Rodriguez, Eva, ar-17-1827.R1 Arthritis & Rheumatology. 2018 Apr 12. doi: 10.1002/art.40521. FI: 9.002

The Editorial Board selected this paper to be highlighted in Journal’s “Clinical Connections” feature, which appears in the front of the print and online issues.

PD-L1 REGULATORY B CELLS ARE SIGNIFICANT DECREASED IN RHEUMATOID ARTHRITIS PATIENS AND INCREASE IN GOOD RESPONDERS. Zacca ER, Onofrio L, Acosta C, Ferrero P, Alonso S, Ramello MC, Montes C, Mussano E, Onetti L, Cadile I, Stancich MI, Taboada Bonfanti MC, Acosta Rodríguez EV, Gruppi A. Frontiers in Immunology. 2018. Oct 1;9:2241. doi: 10.3389/fimmu.2018.02241. FI: 5.51

 

Autoimmunity

Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ" by Cristian Beccaria, María Amezcua Vesely, Facundo Fiocca Vernengo, Ricardo Gehrau, María Ramello, Jimena Tosello Boari, Melisa Gorosito Serrán, Juan Mucci, Eliane Piaggio, Oscar Campetella, Eva Acosta Rodriguez, Carolina Montes, and Adriana Gruppi. Nature Communications. 2018. Apr 24;9(1):1628. doi: 10.1038/s41467-018-04063-5. FI: 12.2

 

Infection

Unconventional Pro-inflammatory CD4+ T Cell Response in B Cell-Deficient Mice Infected with Trypanosoma cruzi. Gorosito Serrán M, Tosello Boari J, Fiocca Vernengo F, Beccaría CG, Ramello MC, Bermejo DA, Cook AG, Vinuesa CG, Montes CL, Acosta Rodriguez EV, Gruppi A. Front Immunol. 2017 Nov 21;8:1548. doi: 10.3389/fimmu.2017.01548. eCollection 2017. FI: 5.6

Tissue tropism of Saint Louis encephalitis virus: Histopathology triggered by epidemic and non-epidemic strains isolated in Argentina. Rivarola ME, Albrieu-Llinás G, Pisano MB, Tauro LB, Gorosito-Serrán M, Beccaria CG, Díaz LA, Vázquez A, Quaglia A, López C, Spinsanti L, Gruppi A, Contigiani MS. Virology. 2017 May;505:181-192. FI: 3.35

Neuronal Degeneration induced by an epidemic strain of Saint Louis Encephalitis virus isolated in Argentina. María Elisa Rivarola , Soledad de Olmos, Guillermo Albrieu-Llinás, Laura Beatriz Tauro, Melisa Gorosito-Serrán,Brenda Salomé Konigheim, Marta Silvia Contigiani, Adriana Gruppi. Frontiers in Microbiology, Section virology. 2018 Jun 7;9:1181. doi: 10.3389/fmicb.2018.01181. FI: 4.076

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 Immunology. 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.

 

Fellows working in CIBICI:

Bioch. LAURA ALMADA - lauraalmadal@gmail.com 

Bioch. YAMILA GAZZONI – ygazzoni@gmail.com

Dr. Maria C Amezcua Vesely - caroamezcuavesely@gmail.com

 

Fellows working in Hospital Nacional de Clínicas-UNC:

Bioch. Paola Ferrero. Chief of ¨Laboratorio de Inmunologia y Serologia¨, HNC ferreropaola@hotmail.com