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Published on: March 6, 2010
Constitutive expression of high levels of soluble mouse CD4 in transgenic mice does not interfere with their immune
S Weber1, A Traunecker, K Karjalainen
1Basel Institute for Immunology, Switzerland.
Insights
Soluble CD4 (sCD4) did not impact T cell development or function in transgenic mice. These findings suggest a low affinity interaction between CD4 and MHC class II in mice, with potential clinical implications for HIV therapy.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- CD4 interaction with MHC class II is vital for T cell development and function.
- Soluble CD4 (sCD4) is explored as a potential therapeutic for HIV infection.
Purpose of the Study:
- To investigate the effects of soluble CD4 (sCD4) on the immune system in vivo.
- To assess the impact of sCD4 on T cell development, function, and immune responses.
Main Methods:
- Generation of transgenic mouse lines expressing monovalent and decavalent mouse sCD4.
- Analysis of T cell populations (CD4+CD8-), T cell responses to stimuli, and in vivo antibody production.
- Comparison of transgenic mice with control littermates.
Main Results:
- Transgenic mice expressing sCD4 showed no significant differences compared to controls.
- Normal development of single-positive CD4+ T cells was observed.
- T helper cell function and in vivo antibody responses remained unaffected by sCD4 expression.
Conclusions:
- The CD4-MHC class II interaction exhibits low affinity in mice.
- sCD4 does not appear to disrupt normal immune system function in this model.
- Findings have implications for the therapeutic use of sCD4 in human immunodeficiency virus (HIV) infection.
Abstract:
Interactions of CD4 with the major histocompatibility complex (MHC) class II molecules are crucial during thymic development and subsequently for the function of single-positive CD4+CD8- T lymphocytes. Here, we have investigated the potential effects of soluble CD4 (sCD4) on the immune system. We generated two different transgenic mouse lines, which constitutively expressed either approximately 100 micrograms/ml of monovalent or approximately 20 micrograms/ml of decavalent mouse sCD4 molecules in their sera. Analysis of these mice revealed no differences compared to control littermates, e.g. the single-positive CD4+ cells developed normally and these cells responded to allogeneic and anti-CD3 antibody stimuli like the cells from control mice. Furthermore, the T helper cell function for antibody responses in vivo were not affected. Our data provide evidence that, in mouse, the CD4-MHC class II-interaction has very low affinity. Since sCD4 is considered to be a therapeutical agent for human immunodeficiency virus infection, these findings are not only of basic, but also of clinical interest.
