The pattern of clinical breast cancer metastasis correlates with a single nucleotide polymorphism in the C1qA component of complement.

Complement is one of primary defense mechanisms against intravascular microorganisms and could play a role in the immune response to malignancy and hence its clinical behavior. We evaluated if the sole coding polymorphism of C1qA associates with outcome in patients with breast carcinoma. Genotyping for C1qA[276A/G] was performed in 63 breast cancer subjects with localized tumor and compared with that in 38 breast cancer subjects with metastasis.

Perspectives in asthma: molecular use of microbial products in asthma prevention and treatment.

Asthma and atopy are characterized by T(H)2-type patterns of inflammation. The hygiene hypothesis suggests that early-life environmental exposure to microbes, other pathogens, and their products promotes innate immune responses that suppress atopy; the current epidemic of allergic disease may result from a dearth of such stimuli. Antiatopic responses engendered by these exposures include both T(H)1-type and regulatory-type patterns, the latter including mechanisms of antigen-presenting cells as well as those of lymphoid origin, and are characterized by prominent IL-10 and/or TGF-beta effects.

C1q: its functions within the innate and adaptive immune responses and its role in lupus autoimmunity.

The complement cascade is a multi-faced effector component of the innate immune response. C1q is the recognition component of the classical pathway of complement activation. In addition, C1q has been recognized to serve a number of other biological functions including a modulating role on cellular functions within the adaptive immune response.