Suppression of mouse contact hypersensitivity after treatment with antibodies to leukocyte function-associated antigen-1 and intercellular adhesion molecule-1

Abstract

We investigated the effects of the antibodies against the adhesion molecules leucocyte function associated antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) on mouse allergic contact hypersensitivity. Mice were injected intraperitoneally with both antibodies before sensitization by an epicutaneous application of dinitrofluorobenzene (DNFB). Simultaneous administration of the antibodies induced suppression of ear swelling in the effector phase of contact hypersensitivity. To show the effect of antibodies in vitro, lymph node cells (LNC) of mice treated with antibodies or with phosphate-buffered saline (PBS) were cultured in the presence of dinitrobenzene sulphonic sodium salts (DNBS), and the production of interleukin-2, interleukin-4 and interleukin-10 in the culture supernatants was measured using an enzyme-linked immunosorbent assay (ELISA). It was found that the production of interleukin-2 in the cells of mice treated with the antibodies was significantly lower than in the cells of PBS-treated mice. On the other hand, no difference was noted in the production of interleukin-4 or interleukin-10. Our results indicate that in vivo simultaneous administration of antibodies to cell adhesion molecules before hapten sensitization induces the suppression of contact hypersensitivity in mice and that the suppression may be due to the inhibition of the production of interleukin-2.

CD155 (PVR/Necl5) Mediates a Costimulatory Signal in CD4+ T Cells and Regulates Allergic Inflammation

“…We showed that treatment with anti-CD155 mAb dampened CHS. Treatment with anti-LFA-1 mAb has been reported to similarly inhibit the development of CHS (42). However, although LFA-1 also mediates a costimulatory signal that leads to Th1 development from naive CD4 + T cells, mice deficient in LFA-1 or treatment of mice with anti-LFA-1 mAb show impaired migration of T cells to draining lymph nodes (43), leading to overall T cell dysfunction.…”

Role of Intercellular Adhesion Molecule–1 and Lymphocyte Function-Associated Antigen–1 During Nonsuppurative Destructive Cholangitis in A Mouse Graft–Versus–Host Disease Model

“…Similar to studies in mice with cutaneous contact hypersensitivity and rheumatoid arthritis patients, IL-4, and IL-10 production in liver of our GVAD model was unaffected by anti-ICAM-1 therapy. [50][51][52] Hence, anti-ICAM-1 appears to selectively decreases IL-2 production and T-cell proliferation in different tissues and mammalian species. The impressive increase in the serum IgE levels (humoral GVHD) in this model are dependent on IL-4 (Howell, unpublished data).…”

New Insights into the Pathomechanisms of Contact Dermatitis by the Use of Transgenic Mouse Models

“…A large number of adhesion molecules has been shown to be an important element in the pathogenesis of CD. Also several molecules involved in antigen presentation, such as major histocompatibility complex molecules or co-stimulatory molecules, are thought to be essential in ACD [Murayama et al, 1997]. On keratinocytes and in the perivascular infiltrates of the CHS response, a marked induction of the intercellular adhesion molecule 1 (ICAM-1) is observed.…”