#Dr franz jackson tn professional
Macrophages and DCs in particular are professional antigen presenting cells with the unique ability to activate naïve cells of the adaptive immune system by displaying components of the processed antigens within the major histocompatibility complex (MHC) on their surface and present them to lymphocytes in the presence of necessary co-stimulatory signals ( Wynn et al., 2013). In fact, an important role of the innate immune system is the activation of the adaptive arm. During danger recognition and antigen processing innate immune cells mature and release various soluble immune mediators called cytokines and chemokines, which drive inflammation and attract adaptive immune cells ( Commins et al., 2010). Phagocytosis is one of the main mechanisms for antigen elimination by innate immune cells. Forming our first-line of defense, this recognition is relatively non-specific and quick, reaching its maximal intensity shortly after antigen encounter without yielding specific immunological memory. Innate immune cells see danger through their germline-encoded pattern recognition receptors (PRRs), which recognize specific molecular structures present on pathogens (so-called pathogen-associated molecular patterns or PAMPs) or produced by damaged cells (so-called damage-associated molecular patterns or DAMPs) ( Amarante-Mendes et al., 2018). natural killer or NK cells) and the humoral complement system ( Artis and Spits, 2015).
The innate immune system is composed of a cellular compartment consisting of mononuclear cells (monocytes/macrophages, mast cells), polymorphonuclear cells (neutrophils, basophils, eosinophils), dendritic cells (DCs), innate immune cells (e.g. The immune system can be divided in two main compartments: the innate immune system and the adaptive immune system. Schematic representation of the structure of the immune system and its major functional features.Ī molecule that is recognized by the immune system is called an antigen, which can be both self and non-self in origin. Further, the importance of discovery of immunological pathways for modifying radiation resilience amongst other research directions in this field is implied. The central conclusion is that ionizing radiation fundamentally and durably reshapes the immune system.
In this review, epidemiological, clinical and experimental data regarding the effects of low-dose radiation on the homeostasis and functional integrity of immune cells will be discussed, as will be the role of immune-mediated mechanisms in the systemic manifestation of localized exposures such as inflammatory reactions. By contrast, the so called low dose radiation therapy displays beneficial, anti-inflammatory and pain relieving properties in chronic inflammatory and degenerative diseases. For example, low doses may permanently alter immune fitness and therefore accelerate immune senescence and pave the way for a wide spectrum of possible pathophysiological events, including early-onset of age-related degenerative disorders and cancer. The cytotoxic effects of high dose radiation are less relevant after low dose exposure, where subtle quantitative and functional effects predominate that may go unnoticed until late after exposure or after a second challenge reveals or exacerbates the effects. Ionizing radiation interacts with the immune system in many ways with a multiplicity that mirrors the complexity of the immune system itself: namely the need to maintain a delicate balance between different compartments, cells and soluble factors that work collectively to protect, maintain, and restore tissue function in the face of severe challenges including radiation damage.
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