Innate-Like B Cells and Their Rules of Engagement

Abstract

Antibodies are an integral part of the immune system. They are produced in response to an infection or insult but are also present prior to any encounter with antigen as so-called natural antibodies. This review focuses on the tissues and cellular origins of natural antibodies. It summarizes recent data showing that B-1 cells, an innate-like B cell population distinct in development, repertoire, and tissue location from the majority conventional or B-2 cells, are the main contributors of natural antibodies in mice in steady state. Furthermore, they show that natural IgM production appears largely confined to B-1 cell populations in the spleen and bone marrow. In contrast, B-1 cells in the body cavities, sites of predominance of this population, harbor B-1 cells that do not constitutively produce antibodies. Instead, these cells act as rapid immune responders that relocate to secondary lymphoid tissues and differentiate to cytokine and antibody-secreting cells shortly after an infection. Thus, the process of B-1 cell response participation is distinct from that of B-2 cell activation as the accumulation of effector B-1 cells does not rely on extensive clonal expansion, but instead on their rapid migration and redistribution, a process that appears under the control of infection-induced innate signals.

Expression of activation‐induced cytidine deaminase enhances the clearance of pneumococcal pneumonia: evidence of a subpopulation of protective anti‐pneumococcal B1a cells

“…These include: origin in the PerC in adults, rapid migration to the spleen to quickly produce IgM antibodies, and expression of CD5, a characteristic marker of B1a cells usually found on T cells, along with the usual B-cell markers like CD19. 2 Relationship of the B1a cell subset resisting pneumonia to conventional immune responses It is likely that AID induces low-level somatic mutations in the V-region DNA of the B1a cell subpopulation that we postulate is associated with rapid clearance of pneumonia, but the stimulus that induced these mutations seemingly before the pneumonia infection 6 is unknown. The very rapid antigen-specific B1a cell response to infection measured at 1-2 days (occurring even at 12 hr) is too short for AID-dependent DNA mutations to occur.…”

“…1,2 However, previous work on contact sensitivity (CS) has shown that a subpopulation of B1a cells can be acted upon by activation-induced cytidine deaminase (AID), leading to Abbreviations: AID, activation-induced cytidine deaminase; APPC, aminophenyl-phosphorylcholine; CFU, colony-forming unit; CS, contact sensitivity; CVF, Cobra venom factor; DTH, delayed-type hypersensitivity; HKP, heat-killed pneumococci; i.p., intraperitoneally; i.t., intratracheally; i.v., intravenously; iNKT, natural killer T cells with invariant Va14 + Ja18 + T cell receptors; NAb, natural IgM antibody; OD, optical density; PC, phosphorylcholine; PerC, peritoneal cavity; s.c., subcutaneously; WT, wild-type…”

B cell subsets are activated and produce cytokines during early phases of Francisella tularensis LVS infection

“…The reason why only B-1a cells are able to internalize F. tularensis microbes can be seen in the development of this B cell subset, whose repertoire is selected to respond rather to pathogen-related than to antigenspecific signals. B-1a cells are also known to relocate into secondary lymphoid organs after activation and to differentiate into cytokine and antibody-secreting cells shortly after an infection [35]. The infection of peritoneal B-1a cells by F. tularensis LVS is significantly accompanied by the expression of activation markers within Fig.…”

Clinicopathologic Features of CD5-Positive Nodal Marginal Zone Lymphoma

“…These cells have been associated with autoantibody production, T-cell regulation, and autoimmune disease. [35][36][37] Compared with B2 cells, B1 cells have been shown to have a unique activation pattern. Rather than clonal expansion, these cells rely on rapid tissue migration and redistribution to achieve cell accumulation at sites of immune stimulation.…”