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Memory B cell
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== Markers == Memory B cells are typically distinguished by the cell surface marker CD27, although some subsets do not express CD27. Memory B cells that lack CD27 are generally associated with exhausted B cells or certain autoimmune conditions such as HIV, lupus, or rheumatoid arthritis.<ref name=":22" /><ref name=":02" /> Because B cells have typically undergone class switching, they can express a range of [[Antibody|immunoglobulin]] molecules. Some specific attributes of particular immunoglobulin molecules are described below: * IgM: Memory B cells that express IgM can be found concentrated in the [[tonsils]], Peyer's patch, and lymph nodes.<ref name=":02" /> This subset of memory B cells is more likely to proliferate and reenter the germinal center during a secondary immune response.<ref name=":3"/> * IgG: Memory B cells that express IgG typically differentiate into plasma cells.<ref name=":3"/> * IgE: Memory B cells that express IgE are very rare in healthy individuals. This may occur because B cells that express IgE more frequently differentiate into plasma cells rather than memory B cells <ref name=":3"/> * IgD only: Memory B cells that express IgD are very rare. B cells with only IgD are found concentrated in the tonsils.<ref name=":02"/> It is important to mention the importance of integration of signalling pathways related to the receptors of BCRs and TLRs in order to modulate the production of the antibodies by the expansion of the memory B cells. Therefore, there are different factors that provide the information in order to secret different types of antibodies. It has been demonstrated that the production of specific-IgG1, anaphylactic-IgG1 and total-IgE depends on the signal produce by [[TLR2]] and [[MYD88|Myd88]]. Moreover, the signal produce by [[TLR4]] when it is stimulated by natterins (protein obtained from ''T. nattereri'' fish venom) accelerates the synthesis of the antibody IgE acting as an adjuvant, as it was shown in an in vivo experiment with mice.<ref>{{Cite journal|last1=Komegae|first1=Evilin Naname|last2=Grund|first2=Lidiane Zito|last3=Lopes-Ferreira|first3=Monica|last4=Lima|first4=Carla|date=2013-08-05|editor-last=Richard|editor-first=Yolande|title=TLR2, TLR4 and the MyD88 Signaling Are Crucial For the In Vivo Generation and the Longevity of Long-Lived Antibody-Secreting Cells|journal=PLOS ONE|language=en|volume=8|issue=8|pages=e71185|doi=10.1371/journal.pone.0071185|issn=1932-6203|pmc=3733974|pmid=23940714|bibcode=2013PLoSO...871185K |doi-access=free }}</ref> The receptor CCR6 is generally a marker of B cells that will eventually differentiate into MBCs. This receptor detects [[chemokine]]s, which are chemical messengers that allow the B cell to move within the body. Memory B cells may have this receptor to allow them to move out of the germinal center and into the tissues where they have a higher probability of encountering antigen.<ref name=":12" /> It has been shown that memory B cells have high level expression of CCR6 as well as an increased chemotactic response to the CCR6 ligand ([[CCL20]]) in comparison with naïve B cells. Nevertheless, the primary humoral response and the maintenance of the memory B cells are not affected in CCR6-deficient mice. However, there is not an effective secondary response from the memory B cells when there is a reexposure of the antigen if the cells do not express CCR6. Therefore we can confirm that CCR6 is essential for the ability of memory B cells to be recalled to their cognate antigen as well as for the appropriate anatomical positioning of these cells.<ref>{{Cite journal|last1=Elgueta|first1=Raul|last2=Marks|first2=Ellen|last3=Nowak|first3=Elizabeth|last4=Menezes|first4=Shinelle|last5=Benson|first5=Micah|last6=Raman|first6=Vanitha S.|last7=Ortiz|first7=Carla|last8=O’Connell|first8=Samuel|last9=Hess|first9=Henry|last10=Lord|first10=Graham M.|last11=Noelle|first11=Randolph|date=2015-01-15|title=CCR6-Dependent Positioning of Memory B Cells Is Essential for Their Ability To Mount a Recall Response to Antigen|journal=The Journal of Immunology|language=en|volume=194|issue=2|pages=505–513|doi=10.4049/jimmunol.1401553|issn=0022-1767|pmc=4282958|pmid=25505290}}</ref>
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