Asset Details
Do you wish to reserve the book?
The Role of Endogenous Interleukin-12 in Resistance to Murine Cytomegalovirus (MCMV) Infection and a Novel Action for Endogenous IL-12 p40
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
The Role of Endogenous Interleukin-12 in Resistance to Murine Cytomegalovirus (MCMV) Infection and a Novel Action for Endogenous IL-12 p40
Do you wish to request the book?
The Role of Endogenous Interleukin-12 in Resistance to Murine Cytomegalovirus (MCMV) Infection and a Novel Action for Endogenous IL-12 p40
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
The Role of Endogenous Interleukin-12 in Resistance to Murine Cytomegalovirus (MCMV) Infection and a Novel Action for Endogenous IL-12 p40
1999
Overview
Biologically active interleukin-12 (IL-12), comprising a 40 kDa subunit (p40) covalently linked to a 35 kDa subunit (p35), is produced in response to a range of infectious stimuli. Here, we demonstrate that mice deficient in either IL-12 p40 (p40-/-) or IL-12 p35 (p35-/-) are susceptible to murine cytomegalovirus (MCMV) infection in terms of survival (Balb/c p35-/-) and viral clearance (Balb/c p35-/- and Balb/c p40-/-), and this susceptibility may be correlated to a deficiency in serum interferon-γ (IFN-γ) levels. These data support a role for endogenous IL-12 in controlling MCMV infection. The IL-12 p40 subunit is produced in excess of IL-12 p35, and to date the function of the excess endogenous p40 has been assumed to be one of IL-12 antagonism, as demonstrated by experiments with exogenous p40 both in vivo and in vitro. We show that Balb/c p35-/- alone are significantly compromised in survival of a sublethal infection and in clearance of virus from the spleen. These mice produce a very early IFN-γ spike (8 h after infection) and an aberrant tumor necrosis factor-α (TNF-α) spike (day 2 after infection). MCMV infection has revealed an altered Balb/c p35-/- phenotype compared with Balb/c p40-/-, and this indicates that endogenous p40 may have an activity independent of and additional to IL-12 antagonism in vivo.
Publisher
SAGE Publications,Mary Ann Liebert, Inc
