Use of a CD6 binding partner and method based thereon
The present disclosure relates to methods for treatment and prevention of disease conditions mediated by T-helper 17 (Th17) and/or T-helper 1 (Th1) T lymphocytes (T cells). In particular, the present disclosure relates to use of anti-CD6 antibody for treatment of disease conditions mediated by auto-reactive Th17 and Th1 T lymphocytes. The methods of the present disclosure further have utility in methods for modulating an immune response by suppressing production of the cytokine IL-23R, thereby decreasing inflammation mediated by Th17 cells.
1. A method of treatment for multiple sclerosis in a subject, wherein the subject in need of such treatment exhibits an increased number of T helper 17 (Th17) cells when compared to a healthy subject, the method comprising:
administering a humanized antibody that specifically binds to D1 of CD6 of the subject and causes a reduction of expression of IL-23R on one or more of monocytes, T helper cells and natural killer cells in a body fluid of the subject, wherein the humanized antibody is the only therapeutic antibody administered; and
monitoring IL-23R expression on blood cells and/or dendritic cells of the subject.
2. The method of claim 1 , wherein the subject in need of such treatment also exhibits an increased number of T helper 1 (Th1) cells when compared to a healthy subject.
3. The method of claim 1 , wherein the humanized antibody is Itolizumab.
4. The method of claim 3 , wherein the humanized antibody causes a reduction of one or more of TNF-alpha, IFN-gamma, IL-6, and IL-17A in a body fluid of the subject.
5. A method of treatment for multiple sclerosis in a subject experiencing an increase in T helper 17 (Th17) cells and T helper 1 (Th1) cells, the method comprising:
administering Itolizumab a humanized antibody that specifically binds to CD6 to the subject, wherein the humanized antibody is the only therapeutic antibody administered; and monitoring IL-23R expression on blood cells and/or dendritic cells of the subject, wherein the treatment causes a reduction of expression of IL-23R and subsequent reduction of Th1 cells and Th17 cells.
6. The method of claim 5 , wherein the Itolizumab causes a reduction of one or more of TNF-alpha, IFN-gamma, IL-6, and IL-17A in a body fluid of the subject.