Enhancing Immunological Memory: Unveiling Booster Doses to Bolster Vaccine Efficacy Against Evolving SARS-CoV-2 Mutant Variants.

A growing number of re-infections with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in previously immunized individuals has sparked discussions about the potential need for a booster vaccine dosage to counteract declining antibody levels and new strains. The protective immunity produced by vaccinations, and past illnesses relies on immunological memory. CD4 + T cells, CD8 + T cells, B cells, and long-lasting antibody responses are all components of the adaptive immune system that can generate and maintain this immunological memory.

STING mediates neuronal innate immune response following Japanese encephalitis virus infection.

Flavivirus-mediated inflammation causes neuronal death, but whether the infected neurons can evoke an innate immune response to elicit their own protection, is unknown. In an earlier study we have shown that neuronal RIG-I, play a significant role in inducing production and release of molecules that are related to inflammation. In this study, using a neuronal cell line, we show that RIG-I acts with STING in a concerted manner following its interaction with Japanese encephalitis viral RNA to induce a type 1 interferon response.

Therapeutic targeting of Krüppel-like factor 4 abrogates microglial activation.

Background: Neuroinflammation occurs as a result of microglial activation in response to invading micro-organisms or other inflammatory stimuli within the central nervous system. According to our earlier findings, Krüppel-like factor 4 (Klf4), a zinc finger transcription factor, is involved in microglial activation and subsequent release of proinflammatory cytokines, tumor necrosis factor alpha, macrophage chemoattractant protein-1 and interleukin-6 as well as proinflammatory enzymes, inducible nitric oxide synthase and cyclooxygenase-2 in lipopolysaccharide-treated microglial cells. Our current study focuses on finding the molecular mechanism of the anti-inflammatory activities of honokiol in lipopolysaccharide-treated microglia with emphasis on the regulation of Klf4.

Particulate antigen induced immune activation influences steroidogenesis in murine lymphoid organs with parallel increase in circulating IL-6.

The effect of sheep red blood cells (SRBC), live Escherichia coli cells administration and interleukin-6 (IL-6) treatment on steroidogenesis in murine lymphoid organs with concomitant changes in serum IL-6 levels were studied in the male Swiss albino mice. From the lymphoid tissue homogenate, the activities of 3betaHSD, 17betaHSD, corticosterone, testosterone and IL-6 levels of serum were estimated. The 3betaHSD activity in murine lymphoid organs, as well as the IL-6 levels in serum increased after administration of SRBC and live E.

Effect of particulate antigenic stimulation or in vivo administration of interleukin-6 on the level of steroidogenic enzymes in adrenal glands and lymphoid tissues of mice with parallel alteration in endogenous inflammatory cytokine level.

To study the effects of sheep red blood cells (SRBC), viable Escherichia coli inoculation and IL-6 administration on steroidogenesis, activities and expression of hydroxy steroid dehydrogenase enzymes (3betaHSD and 17betaHSD) were measured in lymphoid organs of control and infected mice after 3 weeks treatment. Serum testosterone and cytokine levels were also estimated. Reduced expression of 3betaHSD4 was found in the spleen of treated groups as compared to control, whereas the 3betaHSD4 expression was increased in the thymus and lymph gland after stimulation.

Modulation of steroidogenic enzymes in murine lymphoid organs after immune activation.

To study the effects of immune cell activation by a protein antigen or lymphoid tissue derived cytokines on peripheral steroidogenesis activities of 3beta HSD and 17beta HSD was measured in lymphoid organs of control and BSA immunized mice after 3 weeks treatment. We demonstrated the presence of 3betaHSD and 17betaHSD in the lymphoid organs after active immunization. We found elevated serum corticosterone after 3 weeks of antigen administration in presence of CFA and a higher serum IL-6 level that also alter lymphoid tissue cytokine responses like TNF-alpha, IL-12p70, and IL-6, among which IL-12p70 and TNF-alpha down-regulate the activity of steroidogenic enzymes in the thymus during an immune response.

Effects of soluble antigen-induced immune cell activation on steroidogenesis in murine lymphoid organ.

The effect of soluble antigenic (bovine serum albumin, BSA) stimulation to induce steroidogenesis in murine lymphoid organs with concomitant changes in proinflammatory or inflammatory cytokine levels and its implication in the alteration of T-cell response was studied in the mice. Male Swiss albino mice (6-8 weeks old) with average body weight (20 +/- 4 g) were randomly assigned to 3 groups and injected with BSA in presence and absence of Freund's complete or incomplete adjuvant, whereas the control group received only saline. After 3 weeks, animals were sacrificed, and serums as well as lymphoid organs were collected.