Inhibition of CCR6 function reduces the severity of experimental autoimmune encephalomyelitis via effects on the priming phase of the immune response.

Chemokines are essential for homeostasis and activation of the immune system. The chemokine ligand/receptor pairing CCL20/CCR6 is interesting because these molecules display characteristics of both homeostatic and activation functions. These dual characteristics suggest a role for CCR6 in the priming and effector phases of the immune response.

Exploiting 4-1BB costimulation for enhancing antiviral vaccination.

4-1BB, a member of the tumor necrosis factor receptor (TNFR) superfamily, is emerging as an important costimulatory molecule, particularly in the regulation of CD8(+) T cell responses. Costimulation through 4-1BB, such as by utilizing agonistic anti-4-1BB monoclonal antibodies, has been well studied in various tumor models. However, 4-1BB is also an important regulator of antiviral CD8(+) T cell responses.

4-1BBL coexpression enhances HIV-specific CD8 T cell memory in a poxvirus prime-boost vaccine.

We have constructed a recombinant fowlpox virus expressing HIV antigens and the costimulatory molecule 4-1BBL. When included in the boost, but not the prime of a poxvirus prime-boost strategy, 4-1BBL significantly enhanced the anti-HIV T cell response generated to this vaccination in BALB/c mice, as detected by ex vivo IFNgamma ELISPOT responses, intracellular cytokine staining to HIV Gag antigens, and enumeration of Gag-reactive CD8 T cells. 4-1BBL however, is not capable of modulating the CD4 T cell response, nor the antibody response to this vaccination strategy.

Cytokines, skin, and smallpox-a new link to an antimicrobial Peptide.

Patients with atopic dermatitis (AD) have an increased risk of infection with several viruses compared to patients with other inflammatory skin disorders such as psoriasis. In this issue of Immunity, it is found that the cytokine milieu in the skin of AD patients profoundly affects the innate response to vaccinia virus (VV) by blocking production of the antimicrobial peptide LL-37.