CXC chemokine receptor type 4 in systemic lupus

© 2014 Bernatsky et al; licensee Herbert Publications Ltd. This is an Open Access article distributed under the terms of Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0). This permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Dear editor There is increasing interest in the complex links between the immune system and cancer risk. Early data indicated decreased breast cancer risk for women with human immunodeficiency virus (HIV) infection compared to the general population [1]. A case-control study further showed that lower breast cancer risk in women with HIV was significantly and independently linked to infection with HIV strains that bind to CXC chemokine receptor type 4 (CXCR-4) [2]. In most normal tissues, CXCR4 is not generally expressed (or is expressed at very low levels), but is found on some types of cancer cells, including breast cancer. CXCR4 is also expressed on abnormal precancerous breast cells. The authors of the case-control study thus hypothesized that, in women with HIV, involution of the abnormal precancerous cells is mediated by binding of CXCR4. Systemic lupus erythematosus (SLE) is an autoimmune rheumatic disease which is associated with a strikingly decreased risk of certain malignancies including breast cancers [3]. Given the data suggesting that the decreased risk of breast cancer in women with HIV infection is mediated by interactions with CXCR4, we hypothesized that the sera of women with SLE actively binds to CXCR4 antigen, which might invoke a pathway through which the lower breast cancer risk in SLE is mediated.