The role of B-1 cells in inflammation

Abstract

B-1 lymphocytes exhibit unique phenotypic, ontogenic, and functional characteristics that differ from the conventional B-2 cells. B-1 cells spontaneously secrete germline-like, repertoire skewed polyreactive natural antibody, which acts as a first line of defense by neutralizing a wide range of pathogens before launching of the adaptive immune response. Immunomodulatory molecules, such as interleukin-10 (IL-10), adenosine, granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-3, and IL-35 are also produced by B-1 cells in the presence or absence of stimulation, which regulate acute and chronic inflammatory diseases. Considerable progress has been made during the past three decades since the discovery of B-1 cells, which has not only improved our understanding of their phenotypic and ontogenic uniqueness but also their role in various inflammatory diseases including influenza, pneumonia, sepsis, atherosclerosis, inflammatory bowel disease (IBD), autoimmunity, obesity and diabetes mellitus. Recent identification of human B-1 cells widens the scope of this field, leading to novel innovations that can be implemented from bench to bedside. Among the vast number of studies on B-1 cells, we have carried out a literature review highlighting current trends in the study of B-1 cell involvement during inflammation, which may result in a paradigm shift towards sustainable therapeutics in various inflammatory diseases.

B1a Lymphocytes (CD19+CD5+) Deficiency in Patients with Crohn’s Disease and Its Relation with Disease Severity

“…Besides, there is evidence of the production of immunomodulatory molecules by B1 cells, such as interleukin (IL)-10, GM-CSF, IL-3, and IL-35, which regulate inflammatory diseases [31]. …”

The immunoglobulin heavy chain 3′ regulatory region superenhancer controls mouse B1 B-cell fate and late VDJ repertoire diversity

“…[1][2][3][4][5] B1 and B2 B cells differ by their origin, antigen specificity, diversity of the antigenic repertoire, cell surface markers, and tissue distribution. B1 and B2 B cells have a different origin: B1 B cells develop earlier than B2 B cells during fetal development and keep their self-renewal capacity all throughout their life, whereas B2 B cells originate from bone marrow precursors.…”

“…B1 B cells are the major B-cell population in the pleural and peritoneal cavities (almost 50% of total B cells), are rarely detected in the lymph nodes and spleen (;1% of total B cells), and are almost undetectable in bone marrow (,0.1% of total B cells). [1][2][3][4][5] Besides these differences for cell precursors and anatomic locations, B1 and B2 B cells exhibit other important differences during their development and maturation. Compared with B2 B cells, B1 B cells have a specific repertoire of B-cell receptor (BCR) characterized by the production of natural immunoglobulin M (NIgM) frequently polyreactive or autoreactive, with low affinity.…”

“…Compared with B2 B cells, B1 B cells have a specific repertoire of B-cell receptor (BCR) characterized by the production of natural immunoglobulin M (NIgM) frequently polyreactive or autoreactive, with low affinity. [1][2][3][4][5] Compared with B2 B cells, B1 B cells exhibit a marked predisposition for class switch recombination (CSR) toward IgA. Compared with B2 B cells, B1 B cells exhibited a lower hypermutation somatic rate than B2 B cells.…”

“…Compared with B2 B cells, B1 B cells exhibited a lower hypermutation somatic rate than B2 B cells. [1][2][3][4][5] Both B1 and B2 B cells thus produce immunoglobulins, but their cell fate is evidently differently regulated.…”