Introduction:
Two forms of IL-1 have been isolated: Il-1a and IL-1b. They represent the products of two distinct genes and exert their effects by binding to two distinct IL-1 receptor types each with different binding affinities (1,2). The production of IL-1b is one of the most effective mediators of inflammatory reactions primarily produced by activated monocytes and macrophages. Cell wall fragments and toxins from gram-positive organisms can induce TNFa and IL-1b production. A large number of cell types, in addition to monocytes and macrophages, have been shown to produce IL-1, such as Langerhans cells, NK cells, B cell lines, endothelial cells and dendritic cells (3).

Application:
Anti-IL-1b is used to detect IL-1b in human leukocytes by flow cytometry and by immunohistochemistry on cytospots and tissue sections. Determining the cytokine profile of IL-1 producng cells and characterizing the responding cells may be important in the determination of the immune status of various patient groups. It is also applicable for biological studies.
Activities of IL-1 include T cell activation, IL-2 receptor induction, stimulation of pre-B cells and augmentation of IL-1 and IFN-induced activation of NK-mediated cytotoxicity. Also IL-1 has been shown to acelerate wound healing, possibly due to its ability to induce angiogenesis, and fibroblast activation. Since IL-1 is a primary inflammatory mediator, the use of IL-1 antigonists, such as IL-1ra or soluble IL-1 receptors is being investigated as a potential treatment for chronic inflammatory diseases (4).

Specifications:
Clone B-A15, is a murine IgG1 monoclonal antibody which recognizes both natural and recombinant IL-1b. It recognizes intracellular IL-1b in human leucocytes. Anti-IL-1b from clone B-A15, blocks human IL-1b induced proliferation on D10S murine cell line. It is advisable to use a specificity control such as one of the following: 1) unlabelled antibody, 2) recombinant cytokines or 3) mouse isotype control.

Literature references:

1. McMahan et al. 1991 EMBJO J 10: 2821
2. Savage et al. 1989. Cytokine. 1: 23.
3. Oppenheim,B. et al. 1986 Immunology Today. 7: 45.
4. Hooper,J., 1990. J. NIH Res. 2: 49
5. Hamon,Y., et al. 1997, Blood. 90: 2911