Interaksi Sel Penyaji Antigen, Limfosit B dan T, serta Antibodi dalam Respons Imun terhadap Infeksi SARS-CoV-2: Tinjauan Literatur

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Infection A complex immunological response involving defense mechanisms of both the innate and adaptive immune systems triggered by coronavirus 2 (SARS-CoV-2). The purpose of this literature review was to methodically examine the molecular and cellular interactions that determine the clinical course of COVID-19 between antigen-presenting cells (APCs), T lymphocytes (CD4+ and CD8+), B lymphocytes, and neutralizing antibodies. Using a descriptive-qualitative literature review technique, seven scientific journals regarding the immunological response to SARS-CoV-2 were reviewed. The findings of this review suggest that the presentation of antigens via MHC-I and MHC-II is triggered when APCs (alveolar macrophages and dendritic cells) recognize Spike (S) and Nucleocapsid (N) proteins via Pattern Recognition Receptors (PRR). This process stimulates cytotoxic CD8+ T cells and B cells and activates CD4+ helper T cells to produce cytokines (IFN-γ, IL-2). After differentiating into plasma cells, B cells release specific IgM, IgA, and IgG antibodies that block the Receptor Binding Domain (RBD). Loss of regulatory control leads to dysregulation in the form of activation of NLRP3/AIM2 inflammasomes, formation of Membrane Attack Complex (MAC) by the complement system, severe T-cell lymphopenia, and oversecretion of proinflammatory cytokines (IL-6, IL-10, TNF-α), known as cytokine storms, which cause acute respiratory distress syndrome (ARDS). The development of recombinant mRNA/protein-based vaccination techniques and precision immunomodulatory drugs relies heavily on a deep understanding of the dynamics of these cellular interactions.