High school-level immunology teaches us that in response to infection, the immune system can deploy three main lines of defense: 1) innate immunity, where cells such as neutrophils and macrophages eat up pathogens and destroy them; 2) adaptive cellular immunity, where immune cells known as T lymphocytes either produce molecules called cytokines to activate other cell types and coordinate the immune response (helper T lymphocytes) or directly recognize and kill infected cells (cytotoxic T lymphocytes); 3) adaptive humoral immunity, where B lymphocytes recognize the invading pathogen and differentiate into cells producing antibodies that will help neutralize and kill the pathogen.
As one moves from high school- to university- to research lab-level immunology, one discovers that the reality is of course much more complex than that. Our knowledge is constantly reshaped and refined by new studies, and the work by Bermejo and colleagues is one such example: in an article published in May in the scientific journal Nature Immunology, the researchers describe how B lymphocytes can produce a cytokine called IL-17 in response to infection by the parasite Trypanosoma cruzi (which causes Chagas disease).
IL-17 is a molecule important in the fight against infection by extracellular parasites or bacteria; it is however also implicated in the pathogenesis of certain autoimmune diseases such as psoriasis, multiple sclerosis or rheumatoid arthritis. IL-17 is mainly produced by helper T lymphocytes known as Th17 and other immune cells collectively termed innate lymphoid cells.
The data presented by Bermejo and colleagues now shows that B lymphocytes are also a major source of IL-17 in response to infection by Trypanosoma cruzi. The researchers demonstrate that these IL-17–producing B cells are required for the optimal control of parasitemia and overall survival of mice infected by the parasite. Interestingly, they also show that the activating and signaling pathways involved in IL-17 production by B cells seem to be completely different from those described for Th17 and innate lymphoid cells.
So here we are with a new cell type (B lymphocytes) added to the list of cells capable of producing a cytokine (Il-17) important in many immune responses. The next step will be to further explore and define the pathways leading to IL-17 production by these cells. It will also be interesting to know whether B lymphocytes can produce IL-17 in response to infection by other types of pathogens.
If you want to know a bit more about the experimental and molecular details of this study, I wrote a more detailed post about it here when the study was first published. Of course, there is also the full original article, link below (access is not free though).
Trypanosoma cruzi trans-sialidase initiates a program independent of the transcription factors RORγt and Ahr that leads to IL-17 production by activated B cells. Bermejo DA, Jackson SW, Gorosito-Serran M, Acosta-Rodriguez EV, Amezcua-Vesely MC, Sather BD, Singh AK, Khim S, Mucci J, Liggitt D, Campetella O, Oukka M, Gruppi A, Rawlings DJ. Nat Immunol. 2013 May;14(5):514-22. doi: 10.1038/ni.2569
Bermejo DA, Jackson SW, Gorosito-Serran M, Acosta-Rodriguez EV, Amezcua-Vesely MC, Sather BD, Singh AK, Khim S, Mucci J, Liggitt D, Campetella O, Oukka M, Gruppi A, & Rawlings DJ (2013). Trypanosoma cruzi trans-sialidase initiates a program independent of the transcription factors RORγt and Ahr that leads to IL-17 production by activated B cells. Nature immunology, 14 (5), 514-22 PMID: 23563688