| First Author | De Vooght V | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 12 | Pages | e83228 |
| PubMed ID | 24349469 | Mgi Jnum | J:209862 |
| Mgi Id | MGI:5568833 | Doi | 10.1371/journal.pone.0083228 |
| Citation | De Vooght V, et al. (2013) B-lymphocytes as key players in chemical-induced asthma. PLoS One 8(12):e83228 |
| abstractText | T-lymphocytes and B-lymphocytes are key players in allergic asthma, with B-lymphocytes producing antigen-specific immunoglobulins E (IgE). We used a mouse model of chemical-induced asthma and transferred B-lymphocytes from sensitized animals into naive wild type mice, B-lymphocyte knock-out (B-KO) mice or severe combined immunodeficiency (SCID) mice. On days 1 and 8, BALB/c mice were dermally sensitized with 0.3% toluene diisocyanate (TDI) (20 microl/ear). On day 15, mice were euthanized and the auricular lymph nodes isolated. B-lymphocytes (CD19(+)) were separated from the whole cell suspension and 175,000 cells were injected in the tail vein of naive wild type, B-KO or SCID mice. Three days later, the mice received a single oropharyngeal challenge with 0.01% TDI (20 microl) or vehicle (acetone/olive oil (AOO)) (controls). Airway reactivity to methacholine and total and differential cell counts in the bronchoalveolar lavage (BAL) fluid were measured 24 hours after challenge. B-lymphocytes of AOO or TDI-sensitized mice were characterized for the expression of surface markers and production of cytokines. We found that transfer of B-cells obtained from mice dermally sensitized to toluene diisocyanate (TDI) into naive wild type mice, B-KO mice or SCID mice led, within three days, to an acute asthma-like phenotype after an airway challenge with TDI. This response was specific and independent of IgE. These B-lymphocytes showed antigen presenting capacities (CD80/CD86 and CD40) and consisted of B effector (Be)2- (IL-4) and Be1-lymphocytes (IFN-gamma). The transferred B-lymphocytes were visualized near large airways, 24 hours after TDI challenge. Thus, B-lymphocytes can provoke an asthmatic response without the action of T-lymphocytes and without major involvement of IgE. |
