acute inflammatory response to antigenic stimulus

Definition

Target type: biologicalprocess

An acute inflammatory response to an antigenic stimulus. An acute inflammatory response occurs within a matter of minutes or hours, and either resolves within a few days or becomes a chronic inflammatory response. [GO_REF:0000022, GOC:add, ISBN:0781735149]

The acute inflammatory response to antigenic stimulus is a complex and highly orchestrated process involving a cascade of cellular and molecular events designed to eliminate the foreign antigen and restore tissue homeostasis. It is triggered when the immune system encounters an antigen, such as a pathogen, allergen, or foreign protein. The process unfolds in a series of well-defined phases:

**1. Recognition and Initiation:**
- Antigen-presenting cells (APCs), such as macrophages and dendritic cells, recognize the antigen through their pattern recognition receptors (PRRs).
- PRRs bind to pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs) present on the antigen.
- This recognition activates the APCs, leading to the production of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6.

**2. Vascular Changes:**
- Cytokines released by APCs act on nearby blood vessels, causing vasodilation and increased vascular permeability.
- This results in increased blood flow to the site of inflammation, leading to redness and warmth.
- Increased vascular permeability allows fluid, proteins, and immune cells to leak into the surrounding tissues, causing swelling.

**3. Leukocyte Recruitment and Activation:**
- Chemokines, such as IL-8 and CXCL10, are released by APCs and endothelial cells, attracting neutrophils and other leukocytes to the site of inflammation.
- Neutrophils are the first responders and migrate through the vascular endothelium into the inflamed tissue via a process called diapedesis.
- Once in the tissue, neutrophils engulf and kill pathogens through phagocytosis and release reactive oxygen species (ROS), further contributing to tissue damage.

**4. Adaptive Immune Response:**
- APCs carrying the antigen migrate to lymph nodes and present the antigen to T lymphocytes.
- Specific T lymphocytes, recognizing the antigen, differentiate into effector T cells, including cytotoxic T cells (CTLs) and helper T cells (Th1 and Th2).
- CTLs directly kill infected cells, while helper T cells produce cytokines that activate other immune cells, including macrophages and B lymphocytes.
- B lymphocytes differentiate into plasma cells, which secrete antibodies that bind to the antigen, neutralizing its activity and marking it for destruction by other immune cells.

**5. Resolution and Tissue Repair:**
- As the inflammatory response subsides, anti-inflammatory cytokines, such as IL-10 and TGF-β, are released.
- These cytokines promote tissue repair and wound healing.
- Macrophages phagocytose dead cells and debris, further contributing to tissue regeneration.

**6. Immune Memory:**
- Some lymphocytes, particularly memory T cells and memory B cells, persist in the body after the initial response.
- These cells retain the memory of the specific antigen and can rapidly mount a secondary response upon re-exposure to the same antigen, leading to faster and more robust immunity.

The acute inflammatory response is a vital protective mechanism that serves to eliminate foreign invaders and restore tissue integrity. However, when dysregulated, it can contribute to chronic inflammation, leading to various diseases, including autoimmune disorders and cancer.'
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