Contributions
Abstract: P1165
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
Natalizumab (NAT) is a very powerful monoclonal antibody used for the treatment of relapsing-remitting subtype of MS (RRMS). Initially was thought that NAT have a clear mechanism of action: blocks the VLA-4 and prevents the leukocyte migration into the brain. Our study attempted to reveal new peripheral immunological effects of NAT with a focus on a T helper (Th) 17 panel of cytokines.
Material and Methods: We performed an observational study in which 19 RRMS patients treated with NAT and 20 healthy subjects were tested, using a Multiplex method, for serum levels of 15 individual pro-inflammatory and anti-inflammatory cytokines representing Th17 cytokine panel (interleukin[IL]-1β, IL-4, IL-6, IL-10, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-25, IL-31, IL-33, interferon [IFN]-γ, sCD40L, tumor-necrosis factor [TNF]-α). This prospective study explored the serum changes of the cytokines by testing initially and after a mean period of 8.2 months (at least 7 months) of NAT treatment. In the study were included NAT-naïve patients and patients who were on NAT treatment for 1, 2, 3 or more than 4 years.
Results: The highest serum levels of pro-inflammatory cytokines have been found in NAT-naïve patients and we observed a decrease in serum titer with increasing duration of treatment. The lowest serum titers were obtained 2 years after initiation of treatment with NAT. Healthy subjects had lower serum levels of IL-1β, IL-10, IL-17F, IL-21, IL-23, IL-31, IL-33, sCD40L, TNF-α compared to RRMS patients. There was a marked decline in the serum levels of sCD40L, IL-23, IL-17F, TNF-α and IL-31 after a period of 8 month of NAT treatment.
In conclusion, NAT, a VLA-4 blocker has other independent immunological effects like decreasing the serum levels of some pro-inflammatory cytokines.
Disclosure: This study was supported by the internal research Grant of The University of Medicine and Pharmacy Targu Mures, Grant Number 18/2015
Abstract: P1165
Type: Poster
Abstract Category: Therapy - disease modifying - Immunomodulation/Immunosuppression
Natalizumab (NAT) is a very powerful monoclonal antibody used for the treatment of relapsing-remitting subtype of MS (RRMS). Initially was thought that NAT have a clear mechanism of action: blocks the VLA-4 and prevents the leukocyte migration into the brain. Our study attempted to reveal new peripheral immunological effects of NAT with a focus on a T helper (Th) 17 panel of cytokines.
Material and Methods: We performed an observational study in which 19 RRMS patients treated with NAT and 20 healthy subjects were tested, using a Multiplex method, for serum levels of 15 individual pro-inflammatory and anti-inflammatory cytokines representing Th17 cytokine panel (interleukin[IL]-1β, IL-4, IL-6, IL-10, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-25, IL-31, IL-33, interferon [IFN]-γ, sCD40L, tumor-necrosis factor [TNF]-α). This prospective study explored the serum changes of the cytokines by testing initially and after a mean period of 8.2 months (at least 7 months) of NAT treatment. In the study were included NAT-naïve patients and patients who were on NAT treatment for 1, 2, 3 or more than 4 years.
Results: The highest serum levels of pro-inflammatory cytokines have been found in NAT-naïve patients and we observed a decrease in serum titer with increasing duration of treatment. The lowest serum titers were obtained 2 years after initiation of treatment with NAT. Healthy subjects had lower serum levels of IL-1β, IL-10, IL-17F, IL-21, IL-23, IL-31, IL-33, sCD40L, TNF-α compared to RRMS patients. There was a marked decline in the serum levels of sCD40L, IL-23, IL-17F, TNF-α and IL-31 after a period of 8 month of NAT treatment.
In conclusion, NAT, a VLA-4 blocker has other independent immunological effects like decreasing the serum levels of some pro-inflammatory cytokines.
Disclosure: This study was supported by the internal research Grant of The University of Medicine and Pharmacy Targu Mures, Grant Number 18/2015