Adjuvants and formulations: how to make an immunogen from an antigen.

Appropriate adjuvants and formulations improve the immunogenicity of antigens, by increasing both the intensity and duration of immune responses. To that aim, the design and use of adjuvants must obey to the rules regulating physiological responses of the immune system, in particular the long-term development of memory lymphocytes. Here I will briefly discuss the main mechanisms of adjuvanticity at the light of recent knowledge on antigen presentation by B memory lymphocytes, the role of nonspecific stimulation of such cells for memory persistence, and the use of particulate antigens to target B cells, thus facilitating immunological T/B lymphocyte cooperation for getting optimal immune responses.

Rationale for treating human influenza infections by passive transfer of specific antibodies.

The fear of a potential pandemic with a highly pathogenic influenza A virus, such as the avian virus H5N1, has rightly prompted multidisciplinary reflections and calls for better preparedness all over the world. In terms of therapeutic aspects, most of the focus has been on vaccines and antivirals. The present 'opinion paper' intends to discuss a different therapeutic approach, although not mutually exclusive to the two others quoted above.

Infection of dendritic cells (DCs), not DC-SIGN-mediated internalization of human immunodeficiency virus, is required for long-term transfer of virus to T cells.

The C-type lectin DC-SIGN expressed on immature dendritic cells (DCs) captures human immunodeficiency virus (HIV) particles and enhances the infection of CD4+ T cells. This process, known as trans-enhancement of T-cell infection, has been related to HIV endocytosis. It has been proposed that DC-SIGN targets HIV to a nondegradative compartment within DCs and DC-SIGN-expressing cells, allowing incoming virus to persist for several days before infecting target cells.

Dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin (DC-SIGN)-mediated enhancement of dengue virus infection is independent of DC-SIGN internalization signals.

Dengue virus (DV) is a mosquito-borne flavivirus that causes hemorrhagic fever in humans. In the natural infection, DV is introduced into human skin by an infected mosquito vector where it is believed to target immature dendritic cells (DCs) and Langerhans cells (LCs). We found that DV productively infects DCs but not LCs.

CXCR4-tropic HIV-1 envelope glycoprotein functions as a viral chemokine in unstimulated primary CD4+ T lymphocytes.

Interaction of HIV-1 envelope glycoprotein gp120 with the chemokine receptor CXCR4 triggers not only viral entry but also an array of signal transduction cascades. Whether gp120 induces an incomplete or aberrant set of signals, or whether it can function as a full CXCR4 agonist, remains unclear. We report that, in unstimulated human primary CD4(+) T cells, the spectrum of signaling responses induced by gp120 through CXCR4 paralleled that induced by the natural ligand stromal cell-derived factor 1/CXCL12.