Characterization of B-1b cells as antigen presenting cells in the immune response to gp43 from Paracoccidioides brasiliensis in vitro Ana Flavia Grandi Vigna a , Luiz Claudio Godoy a , Sandro Rogerio de Almeida b , Mario Mariano a , Jose ´ Daniel Lopes a, * a Disciplina de Imunologia, Departamento de Microbiologia, Imunologia e Parasitologia, Universidade Federal de Sa ˜o Paulo, Rua Botucatu, 862/4 andar, 04023-900 Sao Paulo, Brazil b e Departamento de Ana ´lises, Clı ´nicas e Toxicolo ´gicas da Faculdade de Cie ˆncias Farmace ˆuticas da Universidade de Sa ˜o Paulo, Sao Paulo, Brazil Received 12 February 2002; accepted 20 March 2002 Abstract Antigen presentation is an essential stage in the development of immune response to a specific antigen. This response can lead to the production of antibodies and/or effector T lymphocyte activation. Macrophages, dendritic cells and B-lymphocytes, among others, act as antigen presenting cells. B-lymphocytes capture antigenic particles through a surface receptor of IgM nature. The interaction IgM-antigen leads to endocytosis of the complex and antigen processing which culminates in presentation of the antigen on the cell surface associated with a class II MHC molecule. At least three B cell subsets, B-1a (Ly-1B), B-1b and B-2, are present in the mouse periphery. B-1a and B1-b cells represent a small population in the adult spleen and are abundant in the peritonial and pleural cavities. It has been demonstrated in our laboratory that B-1b cells spontaneously proliferated in stationary cultures of adherent peritonial cells. Further, that these cells migrate to a non-specific inflammatory focus. Based on these findings, we investigated whether these cells are antigen presenting cells in vitro using as antigenic stimulus gp43 from Paracoccidioides brasiliensis . Results showed that B1-b cells express constitutively high levels of class II MHC and costimulatory molecules inducing an efficient proliferation of gp43 sensitized T lymphocytes. # 2002 Elsevier Science B.V. All rights reserved. Keywords: B-1b cell; Paracoccidioidomycosis; Antigen-presenting cell 1. Introduction The response of helper/inducer T cells to soluble protein antigen (Ag) requires the active participation of a second cell type, the antigen-presenting cell (APC) [1]. One function of the APC is to provide the class II MHC- encoded molecule that the TCR co-recognizes with a peptide Ag. A second APC function is Ag processing. A great deal of evidence indicates that soluble Ag are generally not recognized in their native form, but must be physically modified before T cell recognition [2 /4]. The third APC function is the provision of co-stimula- tory signals to the T cell, i.e. signals distinct from that delivered by the combination of Ag and the class II molecule [5]. The best-accepted and most rigorously characterized co-stimulatory molecules are now consid- ered to be the family of B7 proteins (B7-1 and B7-2). B7 proteins are found on APC and their receptors CD28 and CTLA-4 are expressed on T cells [6]. In the past few years, a wide variety of cell types have been shown to function as APC, like macrophages, B cells [7], vascular endothelial, activated T cell [8], L cell fibroblasts transfected with MHC Class II genes [9] and dendritic cells [10,11]. The most extensively studied APCs are macrophages, B cells and dendritic cells. These cells are likely to be the most important APCs in vivo because they are located in secondary lymphoid tissues where T lymphocyte activation takes place. However, these cells differ from each other in the relative amount of expression of Class II MHC Ags, in binding, uptaking and processing of any given Ag and in their secretion of co-stimulatory factors [12]. These differences could influence the relative efficiency of these cells in the activation of subsets of CD4 T cells. * Corresponding author. Tel.: /55-11-576-4529; fax: /55-11-572- 3328. E-mail address: jdlopes@ecb.epm.br (J.D. Lopes). Immunology Letters 83 (2002) 61 /66 www.elsevier.com/locate/immlet 0165-2478/02/$ - see front matter # 2002 Elsevier Science B.V. All rights reserved. PII:S0165-2478(02)00070-6