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Which Part Of The Adaptive Immune Response Involves B Cells

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Adaptive Immune Responses Associated With The Central Nervous System Pathology Of Gulf War Illness

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Department of Biochemistry and Genetics, La Trobe Institute of Molecular Science, La Trobe University, Bundoora, VIC 3086, Australia

Received: May 30, 2021 / Revised: July 5, 2021 / Accepted: July 9, 2021 / Published: July 10, 2021

Innate Immune System: Video, Anatomy & Definition

Sepsis is a life-threatening medical condition that occurs when the host mounts an uncontrolled or abnormal immune response to an overwhelming infection. It is now widely accepted that sepsis occurs in two simultaneous phases, which consist of an initial phase of immune activation followed by a chronic immunosuppressive phase, leading to the death of immune cells. Depending on the severity of the disease and the pathogen involved, the host’s immune system may not fully recover, leading to ongoing complications after the initial infection. As such, sepsis remains a leading cause of morbidity and mortality worldwide, with treatment options limited to general care in intensive care units (ICU). The lack of specific treatments available for sepsis is primarily due to our limited knowledge of the immunophysiology associated with the disease. This review will provide a comprehensive overview of the mechanisms and cell types involved in inducing infection-induced immune activation of both the innate and adaptive immune systems during sepsis. Furthermore, the mechanisms that lead to immune cell death following immune cell hyperactivation will be explored. Assessment and better understanding of the cellular and systemic responses that lead to the onset of the disease could result in the development of much-needed therapies to combat this relentless disease.

Sepsis currently kills eleven million people each year, disproportionately affecting children, the elderly, pregnant women, and people in low-income countries [1]. Recent studies have shown that one in five deaths worldwide is attributed to sepsis, double the number of deaths believed to be from this disease compared to estimates from previous years [2]. Despite developments in our understanding of the pathogenesis of sepsis, it remains a global health challenge. This is mainly due to associated organ dysfunction, prolonged inflammation, immune suppression and predisposition to secondary infections, which can lead to premature death [3].

In general, sepsis is considered a biphasic disease, but both phases can occur synchronously [4]. The initial hyperinflammatory phase, also known as “cytokine storm,” is described by the overwhelming release of inflammatory molecules by the innate immune system, potentially leading to tissue destruction [5]. Shortly after this increase in inflammation, the immune system weakens, leading to a hypoinflammatory state. Here, the immune system exhibits exhaustion and death of cells of the lymphoid and myeloid lineage, leaving patients immunocompromised [6]. Mass depletion of immune cells leaves patients vulnerable to secondary infection, typically caused by opportunistic nosocomial pathogens such as Acinetobacter baumannii (22.2% of cases), Pseudomonas aeruginosa (10.3% of cases), Candida albicans ( candidiasis; 8.5% of cases) and viruses (>1% of cases) [7, 8, 9, 10, 11, 12]. Secondary infections are typically acquired 48 hours before the initial infection, suggesting that immune paralysis peaks during this period; however, this varies between cases and depends on many factors, i.e. patient comorbidities [13]. Studies that specifically investigated the incidence and impact of secondary infection on clinical outcome showed that opportunistic fungi and bacteria significantly increase in the later phase (>15 days) of sepsis when compared to the early phase (<6 days) [14]. Furthermore, other studies revealed that patients with sepsis who died 3 days or more after ICU admission acquired secondary infections [15]. Furthermore, depending on the severity of the infection causing sepsis, the immune system may never fully recover, leaving patients burdened with prolonged immune dysfunction [16]. As this dysfunction extends to cells of the innate and adaptive immune systems, it is critical to understand the molecules and mediators that act to disrupt normal cellular responses as well as cause their death.

Several new therapies to combat sepsis have been developed, however, deaths from sepsis continue to rise. Thus, antibiotic therapy, resuscitation strategies, blood glucose control and ventilator use remain the only validated actions against this disease [17, 18]. The lack of concrete therapies against sepsis exposes gaps in our knowledge. These limitations are highlighted by multiple drug trials that have failed in the past and, in some cases, increased mortality, largely due to efforts to combat inflammation [19]. It is now known that an increase in inflammatory molecules that signal the critical “kick-start” for the immune system to combat invading pathogens is required, especially during culturable sepsis [4, 20]. Therefore, attacking inflammation may do more harm than good. Furthermore, it is well documented by numerous studies that the main driver of sepsis is the host response to infection rather than the invading organisms themselves [21]. Therefore, understanding the role that immune cells play and how immune cell death occurs during sepsis is essential for the future development of therapeutic tools.

Adaptive Immune System

During the early stages of severe infection, necrotic tissue and microbes release destructive substances into the system, which consist of damage-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs), respectively. These harmful pyrogens cause the rapid activation of a series of membrane receptors known as pattern recognition receptors (PRRs), which include toll-like receptors (TLRs), expressed by cells of the innate immune system [22]. Soon after detection of an infectious agent, first-line defenders, including macrophages, dendritic cells, and neutrophils that express these receptors, become highly proliferative in an attempt to eliminate the overwhelming infection as quickly as possible [23]. Following these events, the adaptive immune system takes effect, leading to the activation of helper and cytotoxic T cells through T cell receptor (TCR) activation. The subsequent differentiation and proliferation of these cells leads to a highly specific adaptive immune response [24].

The innate immune response is triggered immediately after the invasion of a foreign body or antigen. In the case of a gram-negative bacterial infection, one PRR that is activated is TLR4 by lipopolysaccharide (LPS) molecules present on the surface of the bacteria [23]. Upon activation, TLR4 forms a complex with CD14 and MD2, triggering a cascade of intracellular signaling events that lead to the production of transcription factors, mainly NF-κB, Ap-1 and IRF3 [25, 26]. Specific cells equipped with pathogen-sensing components, including endothelial cells, dendritic cells, natural killer cells, monocytes in the blood, and macrophages in the tissues, begin to produce and release an abundance of inflammatory mediators once activated. Critical inflammatory factors include IL-1β, IL-2, IL-6, TNF-α, and chemokines such as prostaglandins, histamine, and IL-8. These molecules target vascular endothelial cells, causing the release of nitric oxide (NO) into the system, in turn increasing vascular permeability [27]. In parallel, circulating neutrophils that express functional receptors such as CXCR1 and CXCR2 receive signals from activated antigen-presenting cells (APCs) at the site of infection, alerting them to the foreign body [28]. At this point, circulating neutrophils mobilize and adhere to the epithelial membrane via L-selectin and integrins in the high-affinity state [29]. Here, neutrophils begin to infiltrate the leaky vessels at the site of infection through the process of extravasation. When in tissue, neutrophils perform their effector functions, which involve degranulation, pathogen phagocytosis and NET formation [30]. Other invading APCs also participate in phagocytosis and presentation of foreign peptides on MHC class II molecules to facilitate clearance [31]. Locally, the coagulation cascade occurs with the positive regulation of coagulation factors that promote platelet aggregation. These processes further amplify the inflammatory response until the infection is resolved [32].

In the case of viral infections, including respiratory infections such as influenza, coronavirus, respiratory syncytial virus (RSV), and rhinoceros virus, innate responses differ from those in bacterial infections. Viral PAMPs activate PRRs such as TLR7, which detect single-stranded RNA (ssRNA) [33]. Following PRR activation, downstream signaling events induce transcription of NF-κB and IRF, upregulating pro-inflammatory and antiviral

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