Enter your Email address:
Wolters Kluwer Health may email you for journal alerts and information, but is committed
to maintaining your privacy and will not share your personal information without
Cassetta, Luca; Cassol, Edana; Kajaste-Rudnitski, Anna; Vicenzi, Elisa; Alfano, Massimo; Poli, Guido
Division of Immunology, Transplantation and Infectious Diseases, San Raffaele University and Scientific Institute, Milano, Italy
After CD4+ T lymphocytes, mononuclear phagocytes were demonstrated to be infected in vivo and infectable in vitro by HIV-1. Unlike T cells, they are relatively resistant to the cytopathic effect of the virus therefore resulting in a persistent state of infection oscillating from latency to active virion production. In addition, macrophages can bud and accumulated ex novo produced virions in intracellular vacuoles of debated nature, a feature that has generated the so-called "Trojan horse" hypothesis on the role of these cells in HIV infection. In this scenario, we have recently observed that polarization of monocyte-derived macrophages (MDM) into classically activated (M1) or alternatively activated (M2a) cells by their “pulsed” stimulation with either TNF-α plus IFN-γ or IL-4, respectively, results in the inhibition of virus replication likely by different mechanisms. While M1-polarization acts at an early, pre-integration level in the virus life cycle, M2a-MDM appear restricted by post-integration mechanisms under intense investigation (E. Cassol, J Immunol. 182: 6237, 2009). Furthermore, M2a cells also express high levels of DC-SIGN that, conversely, facilitate infection and cell-mediated transmission of HIV-1 to CD4+ T cells. Since tissue macrophages, unlike dendritic cells, are mostly residential, M2a-driven DC-SIGN expression may play an important role in the local spreading of infection in mucosal rather than lymphatic tissues. In conclusion, macrophage polarization in vivo is likely to span a spectrum of activated phenotypes that may change their state of permissiveness to infection and profoundly influence their capacity to propagate HIV-1 to neighboring CD4+ cells.
© 2011 Lippincott Williams & Wilkins, Inc.
Colleague's E-mail is Invalid
Your Name: (optional)
Separate multiple e-mails with a (;).
Thought you might appreciate this item(s) I saw at JAIDS Journal of Acquired Immune Deficiency Syndromes.
Send a copy to your email
Your message has been successfully sent to your colleague.
Some error has occurred while processing your request. Please try after some time.
An Existing Folder
A New Folder
The item(s) has been successfully added to "".
Login with your LWW Journals username and password.
Username or Email:
Enter and submit the email address you registered with. An email with instructions to reset your password will be sent to that address.
Link to reset your password has been sent to specified email address.
What does "Remember me" mean?
By checking this box, you'll stay logged in until you logout. You'll get easier access to your articles, collections,
media, and all your other content, even if you close your browser or shut down your
To protect your most sensitive data and activities (like changing your password),
we'll ask you to re-enter your password when you access these services.
What if I'm on a computer that I share with others?
If you're using a public computer or you share this computer with others, we recommend
that you uncheck the "Remember me" box.
Save my selection
Article Level Metrics