Immune Response to Fungal Recognition

Factors produced by pathogens that damage the host.

A change in the arrangement of a promoter region that leads to differential expression of a protein, like flagellin in Salmonella.

Specialized structures found on bacteria, made of pilin protein, involved in attachment to host cells and motility.

A mechanism where pathogens accumulate natural mutations over time, leading to changes in protein structures that are targeted by antibodies. This allows them to evade the immune system by becoming unrecognizable.

A strategy where pathogens mimic host proteins or molecules to avoid immune detection. For example, Campylobacter jejuni can mimic host molecules.

A mechanism where pathogens can resist complement-mediated phagocytosis by producing proteins like Osp that bind to complement factor H, inhibiting its activation and thus preventing killing by the immune system.

A protective layer surrounding bacteria that can resist phagocytosis and hinder complement activation, allowing pathogens to evade the immune system.

Many pathogens employ multiple evasion strategies to outsmart the immune system. This can involve combinations of antigenic variation, molecular mimicry, capsule formation, and other mechanisms.

A protein secreted by some bacteria that cleaves immunoglobulin A (IgA) at its hinge region, rendering it ineffective at the mucosal surface.

Capsules are protective layers that surround certain bacteria, enhancing their ability to cause disease by preventing phagocytosis and complement activation.

A protein produced by Listeria monocytogenes that degrades the phagosomal membrane, allowing the bacteria to escape and replicate in the cytoplasm of host cells.

A protein produced by Listeria monocytogenes that hijacks host cell actin filaments, using them to propel itself towards new cells.

A key component of the innate immune response, macrophages engulf and destroy invading microorganisms, including bacteria.

A cytokine (IL-12) produced by macrophages in response to ingested microorganisms they can't kill, activating NK cells to further combat the infection.

Natural Killer (NK) cells are part of the innate immune system and kill infected cells or tumor cells. Their activation by IL-12 leads to IFN-γ secretion, enhancing macrophage function, and direct killing of infected cells.

This is the immune response driven by T cells and antibodies, playing a critical role in combating intracellular bacteria. IL-12 from phagocytes stimulates a TH1 cell response, leading to IFN-γ secretion and activation of macrophages, increasing their killing power. CD8 T cells (cytotoxic T cells) kill infected cells by recognizing bacterial antigens on Class I MHC molecules.

Specialized receptors on immune cells that detect fungal components like cell walls, triggering immune responses.

A type of PRR found on immune cells that specifically recognizes fungal cell wall components, triggering immune responses.

A type of PRR found on immune cells that recognizes fungal cell walls, leading to immune cell activation and cytokine production.

Immune cells that act as sentries, residing in tissues, detect fungal pathogens through PRRs like TLRs and Dectins.

Cytokines released by activated immune cells to attract and activate other immune cells like neutrophils.

Immune cells that play a crucial role in fighting fungal infections by engulfing fungal cells and releasing toxic substances.

Substances released by neutrophils to kill fungal cells, including reactive oxygen species (ROIs), lysosomal enzymes, and neutrophil extracellular traps (NETs).

A type of immune response involving T helper cells that coordinate other immune cells to fight fungal infections.

A type of PRR found on immune cells that recognizes fungal cell wall components like lipoproteins.

Part of the adaptive immune response that helps fight fungal infections by producing cytokines like IFN-gamma and IL-17.

Specialized immune cells that are activated by PRRs like Dectin-1, TLR2, and Dectin-2, and contribute to the innate immune response against fungi.

Antibodies have a limited role against intracellular bacteria. They can bind to bacterial antigens displayed on infected cells, triggering antibody-dependent cell-mediated cytotoxicity (ADCC). They can also activate complement or act as opsonins, promoting phagocytosis.

Some intracellular bacteria can escape the phagosome, like Listeria monocytogenes. Others prevent phagosome-lysosome fusion, such as Mycobacterium tuberculosis. Some bacteria are resistant to lysosomal enzymes, like Corynebacterium pseudotuberculosis. These mechanisms allow bacteria to survive within host cells.

Endotoxin (LPS), found in the outer membrane of gram-negative bacteria, activates macrophages to release cytokines. It also activates the alternative complement pathway. Gram-positive bacteria can have lipoteichoic acid, similar to LPS.

Exotoxins released by bacteria can either stimulate cytokine release or directly damage host cells (cytotoxic). These toxins contribute to the severity of infections.

Bordetella bronchiseptica and Pasteurella multocida, causing atrophic rhinitis in pigs, produce the toxin PMT. PMT disrupts cell signaling and leads to bone resorption and impaired bone formation.

The innate immune response to extracellular bacteria includes physical barriers like skin and mucosal membranes, and antimicrobial peptides like lysozyme and defensins.

When extracellular bacteria invade tissues, the innate immune system triggers inflammation, complement activation, and phagocytosis. Anaphylatoxins, pro-inflammatory cytokines from phagocytes, and other substances promote inflammation.

Antibodies are the main defense against extracellular organisms. They neutralize bacterial cells and their toxic products, preventing infection.

The immune system's response to fungal infections primarily involves cell-mediated immunity, mainly mediated by T helper 1 (Th1) and Th17 cells. Th1 cells are crucial for the body's defense against intracellular fungi, and they work similarly to how they handle intracellular bacteria. Th17 cells, on the other hand, are more efficient at handling extracellular fungi, leading to inflammation and recruitment of neutrophils to fight the infection.

In addition to the cell-mediated response, antibodies are also essential for fighting fungal infections. These antibodies can effectively neutralize fungal pathogens, make them easier for immune cells to engulf (opsonization), activate the complement system to kill the fungi, and enable antibody-dependent cell-mediated cytotoxicity (ADCC), essentially tagging the fungi for destruction by immune cells.

Fungal pathogens have developed multiple strategies to escape the immune system. Biofilm formation is one method, allowing them to create a protective layer, resist being engulfed by immune cells, and establish a persistent infection. They can also modify their cell walls to hide their antigens from the immune system, making it difficult for the body's defenses to recognize and target them.