B Cell

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B cells, also known as B lymphocytes, play an important role in our survival. They function as part of the adaptive immune system and work by producing the necessary antibodies which are specific to the antigens on the surface of invading pathogens[1]. Early B cell development occurs in the foetal liver, and then throughout adult life, B cells are developed from haematopoietic stem cells found in the bone marrow[2]. that express PAX5 transcription factor. PAX5 is a protein that is encoded in the PAX5 gene that is responsible for encoding for the protein (BSAP) that is expressed at early stages of B cell differentiation.

B cells have receptors on their surface known as 'B cell receptors' (BCR) which bind to foreign antigens and become activated. The activation of the B cell causes it to proliferate and differentiate into either a plasma cell or a memory cell. Plasma cells secrete antibodies; memory cells ensure cells can be quickly reactivated and generate more plasma cells when the cell comes into contact with the same antigen from the primary response. Memory cells are can be activated and generate a secondary response even decades after the primary response occurred. This means there is no need for constant stimulation or re-exposure of the B cell to foreign antigens[3].

A B cell which has not come into contact with a foreign antigen before in its lifespan is called a naive B cell, and when it becomes activated it is a mature B cell. Once B cells mature, they are released from the bone marrow and travel into the lymphatic system. Mature B cells enter germinal centres within the lymph nodes and during proliferation, the genes which encode antibodies undergo somatic hypermutation. This is the process where antibodies become more specific to foreign antigens which means the response will be quicker and more efficient. Specifically, the hypervariable regions undergo mutation at a very high rate in the hope of generating antibodies which bind more tightly to antigens[4]. Somatic hypermutation is only able to occur via key enzymes that allow random mutations across the variable regions, which are then 'fixed' by activation-induced deaminase and DNA repair genes, these amongst other enzymes allow BCR's to have a vast range of genetic coding and therefore enables our immune system to work at a much higher level[5].

B cells which elicit a response to self-antigens are destroyed by apoptosis. If they could be activated, this would lead to autoantibodies being produced and autoimmune disease[6].


B cells require a two signal activation process, so they are not activated accidentally or without reason.

The first signal is generated by the antigen binding to the BCR. BCR-associated Ig alpha and beta, especially the immunoreceptor tyrosine-based activation motif (ITAM) are involved in signalling . The second signal is generated by two different mechanisms depending on which antigen is present. There are two different types of antigen: thymus-dependent antigens (TD) and thymus-independent antigens (TI). T-dependent antigens require a T-helper cell to generate the second signal, whereas T-independent antigens do not.

T-independent antigens such as lipopolysaccharides on bacterial cells bind to toll-like receptors (TLRs) on the surface of the B cell, or cross-linking between BCR and bacterial cell wall constituents occurs. This generates the second activation signal[7]. This results in a rapid primary response, however, antibodies bind less specifically and with less affinity.

T-dependent antigens take in the antigen through receptor-mediated endocytosis. The antigen is processed and displayed as peptide fragments along with the MHC class II molecules on the surface of the B cell. T-helper cells (follicular T-helper cells) bind to this complex via their receptors (TCR) which generates the second signal for the B cell to be activated[8]. The second signal, caused by the interaction between the naïve B cell presenting the MHC molecule and the T-Helper cell occurs via a ligand binding. The T cell presents a CD40L (ligand), which then binds to a CD40 molecule on the B cell. This interaction then activates the T cell to release cytokines that can then bind to the B cell. Both the ligand and cytokine binding to the B cell allow activation[9].


  1. Murphy KM, Weaver C. Janeway's Immunobiology. 9th Ed, USA: W. W. Norton and Company. 2016
  2. British Society for Immunology. B cells. 2016 [cited 20/10/18]; Available from: https://www.immunology.org/public-information/bitesized-immunology/cells/b-cells
  3. Hauser AE, Höpken UE. Molecular Biology of B Cells. 2nd Ed, Elsevier Ltd. 2015
  4. Martin A, Scharf MD. Molecular Biology of B cells. 2nd Ed, Elsevier Ltd. 2015
  5. Murphy KM, Weaver C. Janeway's Immunology. 9th Ed, USA: W. W. Norton and Company. 2016
  6. Arizona State University. Viral Attack. [cited 20/10/2018]; Available from: https://askabiologist.asu.edu/b-cell
  7. Buchta CM, Bishop GA. Toll-like receptors and B cells: functions and mechanisms. Immunologic Research 2014; 59: 1-3: 12-22
  8. Murphy KM, Weaver C. Janeway's Immunology. 9th Ed, USA: W. W. Norton and Company. 2016
  9. Murphy KM, Weaver C. Janeway's Immunology. 9th Ed, USA: W. W. Norton and Company. 2016
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