“ACQUIRED IMMUNITY DOES NOT CAUSE THE TISSUE INJURY AS INNATE IMMUNITY” Role of Innate and Acquired Immunity.

  

“ACQUIRED IMMUNITY DOES NOT CAUSE THE TISSUE INJURY AS INNATE IMMUNITY”

 

·        Acquired Immunity:

Acquired Immunity is the immunity that is developed by the host after exposure to some sort of microorganism or suitable antigen. It can also be developed by the transfer of antibodies from an immune donor. Acquired Immunity develops throughout life. [1]

·        Innate Immunity:

Innate Immunity is the defense system that a person is born with. It is the first line of defense and provides a critical mechanism for the rapid sensing and elimination of pathogens. Furthermore, it also involves barriers that prevent foreign substances from entering our bodies.

·        Tissue Injury:

Tissue Injury refers to the injury of the soft tissue resulting from trauma or overuse of muscles, ligaments, or tendons. It can also be caused by medical treatments such as radiation.

Acquired Immunity Does Not Cause Tissue Injury As Innate Immunity

Immune Response after Tissue Injury:

A successful inflammatory response eliminates the trigger followed by a resolution of inflammation and tissue repair by numerous anti-inflammatory cytokines as well as lipid mediators.

Role Of Innate Immune System In Tissue Injury:

 

When a tissue is injured, it disrupts tissue homeostasis and stimulates the innate immune system, resulting in the migration of many immune cells to the injury site. To create an inflammatory environment, these immune cells produce cytokines, growth factors, and enzymes. The main aim of such inflammation is to resolve the infection, repair the tissue damage, and regain the state of tissue homeostasis. [3]  It is a  subsequent complex response, designed to limit further damage and induce healing.

Trauma triggers a series of quick innate immune responses in an attempt to eliminate injured tissues, followed by the activation of repair mechanisms with the ultimate objective of returning cells and tissues to their pre-injury state.

'Non-self' pathogen-associated molecular patterns (PAMPs) from infectious agents (bacteria, viruses, and fungi), as well as the release of large amounts of self-damage-associated molecular patterns (DAMPs) such as ATP, HMGB-1, matricryptins, cold-inducible RNA-binding protein, histones, and mitochondrial DNA is indicated in case of severe injury. [4]

These DAMPS AND PAMPS are also referred to as danger signals. These signals induce local inflammation by the activation of the transcription factors NF-κB or interferon-regulatory factors. TLRs activate tissue-resident macrophages and promote the expression of chemoattractants for neutrophils, monocytes, and macrophages They also induce the expression of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α), IL-1β, and IL-6.

Neutrophils are the first circulating immune cells recruited to the site of injury, promoting inflammation and monocyte/macrophage recruitment. The inflammation is initially maintained by pro-inflammatory M(IFN-γ) macrophages, before being eventually resolved with the help of M(IL-4) macrophages. 

Macrophages and their various phenotypes play a predominant role in the restoration of tissue homeostasis by clearing away cellular debris, remodeling the extracellular matrix (ECM), and synthesizing multiple cytokines and growth factors. 

Apoptotic cells released after tissue injury promoted angiogenic properties of macrophages by releasing prostaglandin E2, which induced endothelial-derived progenitors to angiogenesis and vascular repair during tissue regeneration.

 

Role Of Adaptive Immune System :

Followed by the innate Immune system, The adaptive Immune system is activated. Adaptive immunity plays a critical role during tissue repair and regeneration, especially by The T cells.

T cells are capable of secreting a diverse range of cytokines and growth factors, which have beneficial or inhibitory effects on tissue healingCD4⁺ Tregs are critical for the repair and regeneration of several tissues including skin, bone, lungs, kidney, skeletal muscle, and cardiac muscle.

The presence of Tregs; a specialized subpopulation of T cells that act to suppress the immune response, thereby maintaining homeostasis and self-tolerance, results in the production of arginase and anti-inflammatory cytokines such as IL-10 and TGF-β. These released substances create an anti-inflammatory environment that allows macrophages to repair and polarise. Treg levels stay elevated even as conventional T cells depart. This could be due to Tregs expressing epithelial growth factor receptor (EGF-R) in visceral adipose, muscle, and the lamina propria. Mast cells release the growth factor amphiregulin, which permits EGF-R to keep Tregs in the injured region. Tregs proliferate and upregulate amphiregulin secretion, which is required for regeneration. [5]

 

 

CONCLUSION :

Yes, Acquired immunity does not cause tissue injury as innate immunity because innate immunity produces inflammation by the recruitment of several immune cells at the site of injury. These immune cells secrete cytokines, growth factors, and enzymes to establish inflammation. Whereas the Acquired immune system mainly possess anti-inflammatory property to establish homeostasis and promote tissue regeneration