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Adult Still\\\'s disease (ASD) is a auto inflammatory disease so-called polygenic. ASD is a rare pathology known as benign, its diagnosis remains a diagnosis of elimination based on the set of polymorphic clinical signs (fever, rash and or arthralgia), with 2 forms, systemic and articular. Thus, in the absence of a specific diagnostic marker, the ASD remains a diagnosis of elimination. The interaction between ASD and pregnancy is poorly known, the literature is still poor given its rarity, the number of published observations does not exceed thirty, so its discovery during pregnancy can may compromise the outcome of pregnancy, rarely a life-threatening of the mother.disease flares can occur during ASD in the 2nd trimester and in the postpartum. Corticosteroid therapy is the first-line treatment of ASD, probably more effective in systemic forms of the disease. We recall here this pathology through the case of a patient who during 10 years of evolution of MSA, in its corticodependent systemic form, had carried out 3 pregnancies without resonance or dysgravidia.

This study was done to determine the release of cytokines (IL-6, IL-8 and TNF) in stored whole blood. Fifty (50) samples were collected from 50 subjects for the study. These comprise of 25 males and 25 females. The subjects comprise of adults aged 18-40 years with 29 years as the mean age. The study was conducted at GEM Research Laboratories. The IL-6, IL-8 and TNF were assayed respectively for all subjects on 0 day, 14th day and 35th day. The mean levels of IL-6, IL-8, and TNF were 10.68 pg/ml, 3.40 pg/ml, and 1.43 pg/ml respectively for 0 day, 7.56 pg/ml, 16.52 pg/ml, and 7.88 pg/ml respectively for 14th day, and 5.12 pg/ml, 124.24 pg/ml, and 59.08 pg/ml respectively for 35th day. Significant statistical difference (p<0.05) was observed in IL-6 and IL-8 mean levels across all groups (0/14th day, 0/35th and 14th/35th day) compared except in 0/14th where TNF mean levels showed no significant statistical difference (p>0.05). We recommend pre storage white cell reduction for whole blood and all red cell components.

The immune system\'s intricate interplay with tissue regeneration during pregnancy stands as a captivating field of scientific inquiry, offering profound insights into both maternal physiology and regenerative medicine. This review synthesizes current knowledge on the multifaceted roles of the immune system in orchestrating tissue repair throughout gestation. From the establishment of pregnancy to fetal development, an array of immune cells, cytokines, and signaling pathways collaborates to create a conducive environment for tissue regeneration. Throughout pregnancy, the immune system demonstrates a delicate equilibrium, balancing tolerance towards the fetus while ensuring protection against pathogens. Key immune cell populations such as macrophages, natural killer cells, and regulatory T cells dynamically contribute to tissue repair by modulating inflammation and promoting angiogenesis. Furthermore, cytokines and growth factors, including interleukins and TGF-?, play pivotal roles in regulating cell behavior and extracellular matrix remodeling, thereby influencing tissue regeneration. Understanding these immune-mediated mechanisms in pregnancy has significant implications for regenerative medicine. Insights gleaned from the unique immune adaptations during gestation offer potential avenues for innovative therapeutic interventions in wound healing, organ regeneration, and various pathological conditions.

Co-infection with HIV and malaria presents a multifaceted clinical scenario with intricate immunological interplays, wherein neutrophils, the primary mediators of innate immunity, emerge as pivotal actors. This paper aims to comprehensively analyze the dynamic role of neutrophils in the progression of HIV within the context of malaria co-infection. Neutrophils, conventionally viewed as short-lived effectors, exhibit remarkable plasticity and multifunctionality, contributing significantly to immune responses during co-infections. Their phenotype and functions undergo profound alterations in response to the complex milieu of both HIV and malaria, impacting disease progression and immunomodulation. This paper scrutinizes the nuanced alterations in neutrophil phenotypes, their diverse effector functions, and their contributions to immunopathogenesis within the HIV-malaria co-infection paradigm. Neutrophils, driven by dysregulated cytokines and inflammatory cues, exhibit heightened activation, potentially exacerbating tissue damage and chronic immune activation. Insights gleaned from understanding neutrophil dynamics in this co-infection scenario hold significant therapeutic implications. Potential interventions targeting neutrophil responses offer promising avenues for modulating immune dysregulation and managing disease progression. The review underscores the need for innovative therapeutic approaches aimed at harnessing neutrophil functionalities to mitigate HIV progression within malaria co-infected individuals. In conclusion, unraveling the intricate roles of neutrophils provides critical insights into the immunopathogenesis of HIV within the context of malaria co-infection. This comprehensive understanding not only sheds light on immune modulation but also presents a foundation for future therapeutic strategies aimed at improving clinical outcomes in this complex co-infection scenario.