12.1 Immunity to Viruses and Parasites

The body's natural defense system that rapidly responds to pathogens. It involves cells like macrophages and neutrophils, and proteins like complement. This response is non-specific, meaning it acts against a wide range of pathogens.

A group of proteins that work together to destroy pathogens. They can directly kill bacteria or attract immune cells to the site of infection.

A process where immune cells engulf and destroy invading pathogens. This is a crucial part of innate immunity.

A type of immune cell that is a master of phagocytosis. They are the first responders to infection, quickly engulfing and destroying bacteria.

These are white blood cells that can engulf and destroy pathogens. They are also involved in antigen presentation, which helps activate adaptive immunity.

Bacteria that live and replicate outside of host cells. They can cause disease by damaging tissue directly or releasing toxins.

The ability of pathogens to evade the host's immune system, allowing them to survive and multiply.

Pathogens that can cause disease by directly killing host cells or releasing toxins.

Cells like macrophages and dendritic cells release signaling molecules called cytokines during inflammation. These cytokines attract more immune cells to the site of infection.

Innate lymphoid cells (ILCs) are a type of immune cell that directly releases signaling molecules like IL-17 and IL-22, attracting neutrophils to fight off bacteria.

Antibodies, specifically IgG, IgM, and IgA, play a crucial role in fighting extracellular bacteria. They act like blockers, preventing bacteria from causing infection.

CD4+ helper T cells are important for coordinating the immune response against extracellular bacteria. They release signaling molecules (cytokines) that activate other immune cells and promote antibody production.

Excessive or uncontrolled inflammation caused by the body's response to bacteria can damage tissues. This occurs when immune cells release harmful substances like reactive oxygen species (ROS) that destroy cells and tissues.

Sepsis is a body-wide inflammatory response to infection, triggered by cytokines like TNF, IL-6, and IL-1. It can disrupt blood flow, clotting, metabolism, and organ function, potentially leading to septic shock, the most severe form.

Superantigens are bacterial toxins that activate a large number of T cells, causing an exaggerated and uncontrolled immune response. This can lead to tissue damage and systemic inflammation.

After a streptococcal infection, the body can sometimes produce antibodies that react with its own tissues, leading to conditions like myocarditis (heart inflammation) and glomerulonephritis (kidney inflammation). This happens because some antibodies recognize similar structures in both bacteria and human tissues.

Some bacteria, like those with polysaccharide capsules, have evolved mechanisms to evade the immune system. These capsules can prevent phagocytosis by immune cells, and some bacteria contain sialic acid that inhibits complement activation, a part of the immune response.

Bacteria can change their surface antigens to escape the body's immune memory. This is a common way for bacteria to evade humoral immunity, which relies on antibodies specific to certain antigens. They can also release antigens in membrane blebs, diverting antibodies away from the bacteria itself.

A mechanism where viruses change their surface antigens to evade the immune system's recognition.

Viruses can inhibit the presentation of viral antigens to the immune system by blocking MHC molecules.

Certain viruses produce molecules that directly suppress immune responses, like cytokines.

Chronic viral infections can lead to exhaustion of T cells, making them less effective at fighting the virus.

Parasites have complex life cycles, often involving multiple hosts, making it harder for the immune system to eliminate them.

The innate immune system's main weapon against protozoa is phagocytosis, but many protozoa resist this defense mechanism.

The body's primary defense against protozoa surviving inside macrophages is cell-mediated immunity, involving Th1 cells.

Eosinophils play a key role in the innate immune response to helminths, while neutrophils and macrophages are less effective due to the parasite's thick tegument.

Protozoal pathogens can stimulate the production of specific antibodies (B cell mediated) and cytotoxic T lymphocytes (T cell mediated) to combat infection.

IFN-γ, a type of interferon, plays a crucial role in protecting the body from various protozoal infections.

Defense against many helminthic infections is mediated by the activation of Th2 cells, which then produce IgE antibodies. These antibodies bind to the Fcε receptor of eosinophils and mast cells, leading to the activation of eosinophils, which destroy the helminths.

Parasites can evade the host's immune system by changing their surface antigens. For example, malaria parasites express different antigens during different stages of their life cycle.

Parasites can evade the host's immune system by continuously changing their major surface antigens, making it difficult for the immune system to recognize and target them.

Intracellular bacteria survive and replicate within phagocytes, making them inaccessible to circulating antibodies. Their elimination requires cell-mediated immunity.

Phagocytes and NK cells are key players. TLRs and NLRs recognize bacteria, activating phagocytes. IL-12 and IL-15 activate NK cells, which are also activated by NK cell-activating ligands expressed on infected cells.

CD4+ T cells activate phagocytes through CD40 ligand and IFN-γ, leading to microbe killing. CD8+ CTLs directly kill infected cells.

A strong immune response against intracellular microbes can sometimes damage tissues.

Neutrophils, macrophages, and ILCs are vital. Macrophages and dendritic cells recognize β-glucans on fungi using TLRs and dectins. They release cytokines to recruit and activate neutrophils. Neutrophils phagocytose and kill fungi with ROS and lysosomal enzymes.

CD4+ T cells activate macrophages and neutrophils for intracellular killing. CD8+ T cells directly lyse fungal-infected cells. Extracellular fungi trigger a Th17 response to attract neutrophils.

Viruses are obligate intracellular pathogens that replicate using host machinery, disrupting cell function and leading to cytopathic effects.

Type I interferons inhibit viral replication, and NK cells kill infected cells. Plasmacytoid DCs and infected cells secrete type I IFNs, which block viral replication. NK cells recognize activating ligands on infected cells and eliminate them.

Antibodies neutralize viruses during their extracellular phase by blocking binding and entry, promoting phagocytosis, and activating complement. CTLs eliminate intracellular viruses by killing infected cells.

Viral antigens are presented by APCs to CD8+ T cells, which differentiate into CTLs. CTLs recognize and kill virus-infected cells displaying the same antigen through MHC I.

These bacteria can multiply outside of host cells, for example, in the blood, connective tissues, and the spaces within the respiratory and digestive tracts.

These bacteria can cause damage by directly harming host cells or by releasing toxins that cause tissue damage.

The body's first line of defense against extracellular bacteria, this involves a group of proteins that can directly kill bacteria or attract immune cells to the infection.

These cells can capture and destroy extracellular bacteria. They have special receptors that help them recognize bacteria.

Immune evasion refers to the ability of pathogens to escape the body's immune system, allowing them to survive and multiply.

This type of immune response is specific to a particular microbe. It is a slower, more complex response but provides long-term protection.

Antibodies, specifically IgG, IgM, and IgA, play a crucial role in fighting extracellular bacteria. They act like blockers, preventing bacteria from causing infection.

These cells are critical for coordinating the immune response against extracellular bacteria. They activate other immune cells and promote antibody production.

Antibodies target extracellular bacteria by blocking infections, eliminating microbes, and neutralizing toxins.

CD4+ helper T cells stimulate immune responses against extracellular bacteria by releasing cytokines, enhancing phagocytosis, and promoting antibody production.

The main damaging effects of the immune response to extracellular bacteria include inflammation caused by ROS and lysosomal enzymes, and excessive immune activation leading to tissue damage.

A potent immune response against intracellular microbes can sometimes cause collateral damage to host tissues.

Intracellular bacteria reside and multiply inside phagocytes, making them inaccessible to circulating antibodies, thus requiring cell-mediated immunity (T cells) for their elimination.

The innate immune response against intracellular bacteria primarily involves phagocytes and NK cells. TLRs and NLRs identify bacteria, activating phagocytes, and IL-12/IL-15 activate NK cells.

CD4+ T cells stimulate phagocytes through CD40 ligand and IFN-γ, resulting in microbial death. CD8+ CTLs directly destroy infected cells.

Fungal infections are known as mycoses. Many are opportunistic, affecting immunocompromised individuals. Fungi can exist extracellularly or inside phagocytes.

Neutrophils, macrophages, and ILCs are key players in innate immunity against fungi. Macrophages/dendritic cells recognize β-glucans using TLRs and dectins, releasing cytokines to recruit and activate neutrophils.

CD4+ T cells activate macrophages and neutrophils for intracellular fungal killing. CD8+ T cells directly destroy infected cells. Extracellular fungi trigger a Th17 response for neutrophil recruitment.

Viruses, obligate intracellular pathogens, replicate using host cell machinery, disrupting cell function and causing cytopathic effects.

Type I interferons inhibit viral replication, and NK cells kill infected cells. Plasmacytoid DCs and infected cells release type I IFNs, blocking viral replication. NK cells recognize activating ligands on infected cells and eliminate them.

Antibodies neutralize viruses during their extracellular phase by blocking binding and entry, promoting phagocytosis, and activating complement. CTLs eliminate intracellular viruses by killing infected cells.

Viral antigens are presented by APCs to CD8+ T cells, which differentiate into CTLs. CTLs recognize and kill virus-infected cells displaying the same antigen through MHC I.

Certain viruses produce molecules that directly suppress immune responses, often by interfering with the signaling pathways of immune cells.

Some protozoa change their antigens during different life stages, making it hard for the immune system to recognize and fight them. For example, the malaria parasite's sporozoites are antigenically distinct from the merozoites that cause chronic infection.

To evade the immune system, some parasites continuously change their major surface antigens, making it tricky for the body's defenses to keep up.

Immune evasion strategies employed by parasites are quite diverse.

IFN-γ, a potent immune signaling molecule, plays a key role in protecting the body from various protozoal infections.