Block 3: IMM (DITKI) ADAPTIVE IMMUNITY - HUMORAL RESPONSE

Innate Immunity

• Pathogen recognition is a key function of the innate immune system, allowing it to distinguish between self and non-self.
• Pattern Recognition Receptors (PRRs) on immune cells recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).
• PAMPs are unique to pathogens, while DAMPs are released from damaged cells.
• Toll-like Receptors (TLRs) are a major class of PRRs, each recognizing specific PAMPs.
• TLR activation triggers signaling pathways that induce inflammatory responses, leading to the production of cytokines, chemokines, and other immune effectors.
• Surfactant collectins, such as surfactant protein A (SP-A) and surfactant protein D (SP-D), are soluble PRRs that bind to pathogens, facilitating their clearance and promoting inflammatory responses.

Adaptive Immunity

• T cell activation involves a complex interplay of signals, including antigen recognition by the T cell receptor (TCR) and co-stimulatory signals.
• MHC molecules present processed antigens to T cells, a key step in recognizing and responding to pathogens.
• CD28, a co-stimulatory receptor, plays a crucial role in T cell activation.
• CTLA-4 is a negative regulator of T cell activation that prevents excessive immune responses.
• Regulatory T cells (Tregs) suppress immune responses, contributing to maintaining immune tolerance and preventing autoimmune reactions.
• Superantigens are potent activators of T cells, leading to massive cytokine release and potentially severe immune dysregulation.

Macrophages

• Macrophages are highly plastic cells, able to differentiate into various subtypes depending on the environmental cues they receive.
• M1 macrophages are pro-inflammatory, while M2 macrophages are anti-inflammatory and contribute to tissue repair.
• Macrophages play a critical role in both innate and adaptive immunity, engulfing pathogens, presenting antigens to T cells, and releasing cytokines that shape the immune response.

Granulomas

• Granulomas are a type of inflammatory structure formed in response to chronic infections, such as tuberculosis.
• Granulomas contain a central core of infected cells surrounded by a layer of macrophages and other immune cells.
• Foamy macrophages are a characteristic feature of granulomas in tuberculosis, reflecting the accumulation of lipids within these cells.
• Granulomas can be either protective, containing and preventing the spread of the infection, or destructive, contributing to tissue damage.

Asthma

• Asthma is a chronic airway disease characterized by inflammation and bronchospasm.
• Chronic inflammation involves T-cell activation, cytokine release, and airway remodeling.
• Airway remodeling includes changes in the structure of the airways, such as thickening of the airway walls and increased mucus production.

Wound Repair

• Wound repair is a complex process involving multiple cell types and signaling pathways.
• Vascular Endothelial Growth Factor (VEGF) is a key regulator of angiogenesis, the formation of new blood vessels, which is essential for wound healing.
• Macrophages play a crucial role in wound repair, clearing debris, promoting angiogenesis, and contributing to tissue regeneration.