We have found higher c-value for Rho/Cdc42 in an unperturbed TCR signaling pathway. In contrast, it has become 0 and 0.31557 in a pathogen perturbed system and in the system, where it is optimized for two conflicting objective functions, respectively. Excessive interferon gamma release due to SEB has been linked with the development of a lifethreatening systemic inflammation. We can find its similarity with our results in the form of higher c-value for IFN-c in an infected TCR signaling pathway. It should be mentioned here that repeated injections of enterotoxin in mice resulted in high levels of IL-10, but there was also a dramatic decrease in all the other cytokines. A study by Ackermann et al. in human leukaemic mast cells demonstrated that SAg stimulation downregulates the production of IL-4. Thus, through these findings we can say that SAgs may also downregulate cytokine production. Similarly, Wang et al. has shown that CARMA1 functions as a scaffold protein to recruit PKC-h, Bcl10, and IKKb to the lipid rafts of the immunological synapse, which ultimately leads to the activation of NF-kB. A study by Narayan et al. showed that CARMA complex is required for the induction of NF-kB by AKT, along with PKC activation using a CARMA1-deficient T cell line. AKT has a role in NF-kB induction in T cells. It is here to be mentioned for information that AKT acts upstream of the IKK complex to increase IKK activation, IkB degradation and NF-kB nuclear entry. The AbMole Diperodon c-values for AKT1 was lower in an unperturbed TCR signaling pathway, whereas, it was higher in perturbed one and again lower in an integrated pathway which was optimized for two conflicting objective functions. The case is similar with IKK complex, where c-value is lower in an unperturbed TCR signaling pathway, which later has AbMole Folic acid increased in a perturbed TCR signaling pathway. It has again decreased in an integrated pathway which was optimized for two conflicting objective functions. MALT1 is recruited to the lipid rafts of the immunological synapse following activation of TCR and CD28 coreceptor. This recruitment is dependent on CARMA1. MALT1, Bcl10, and CARMA1 form a trimolecular complex. Expression of a MALT1 deletion mutant has shown to completely block the CD3/CD28 costimulation-induced NF-kB activation. Considering the above experimental evidences for CARMA complex, we have also found lower c-value for CARMA complex in an unperturbed TCR signaling pathway. In contrast, it has become 0.81185 and 0.23229 in pathogen perturbed system and in the system, where it is optimized for two conflicting objective functions, respectively. NCK plays a pivotal role in TCR-induced reorganization of the actin cytoskeleton and the formation of the immunological synapse in T lymphocytes.