Hypothesized asthma cascade in hapten immune contact sensitized mice, consist of B-1 cell- to immunoglobulin M- (IgM) to complement-driven airway responses

Hypothesized asthma cascade in hapten immune contact sensitized mice, consist of B-1 cell- to immunoglobulin M- (IgM) to complement-driven airway responses. The postulated cascade of events are shown from immunization to airway antigen challenge in order to elicit airway hyper-reactivity (AHR) just 1 day later. Trinitrophenyl (TNP) hapten skin contact immunization (upper left) activates TNP antigen-specific B-1 cells in pleural and peritoneal cavities to migrate to the lymphoid tissues. There, the B-1 cells probably mature into cells that secrete IgM which enter the systemic circulation (centre). Then, subsequent TNP airway challenge at 1 day results in the formation of local immune complexes of anti-TNP IgM binding with TNP-self conjugates formed in the airway tissues. These antigen–antibody complexes (upper right) activate complement, and component C5 generates C5a. The C5a (lower right) then either directly binds and activates C5a receptors in the airways, or acts indirectly by activating local mast cells or platelets via their C5a receptors to release bronchoconstrictive mediators. Either pathway then induces an immediate airway response (IR) peaking at 15–30 min and subsequent AHR measured at 24–48 hr (lower right).

Publication

Airway hyper-reactivity mediated by B-1 cell immunoglobulin M antibody generating complement C5a at 1 day post-immunization in a murine hapten model of non-atopic asthma. (2004) Ivana Kawikova, et al. Immunology. 2004 Oct;113(2):234-245. Figure: F6. Homo sapiens

Disease mentions