Innate and Adaptive Immunity: Pathogen Recognition, Collateral Damage, and Virulence Genes

How do innate immune cells recognize potential pathogens?

Innate immune cells express pattern recognition receptors that detect PAMPs (pathogen-associated molecular patterns), which are microbial structures not found on host cells.

What is an example of a pattern recognition receptor?

TLR4 on macrophages recognizes LPS, triggering inflammation.

What is the role of complement in the immune response?

Complement mainly targets extracellular bacteria and pathogens, binding directly to surfaces and inhibiting them by opsonization, inflammation, or direct lysis.

What is the role of interferons in the immune response?

Interferons target intracellular pathogens, inhibiting them by inducing an antiviral state that blocks replication.

Which immune response has the greatest potential for collateral damage to self-tissues?

Complement has greater potential for collateral damage because it acts directly on cell surfaces and triggers inflammation and cell lysis.

What is the humoral component of the adaptive immune response?

The humoral response is mediated by B-cells that recognize specific antigens through their receptors, undergo clonal expansion, and differentiate into plasma cells that secrete antibodies.

How do antibodies influence attachment and colonization by bacteria and viruses?

Antibodies bind specifically to bacterial or viral surface agents, blocking adhesion molecules or viral attachment proteins, preventing pathogens from attaching to host cell receptors.

How do antibodies interact with immune cells and complement?

Antibodies bound to pathogens act as opsonins, allowing PMNs and macrophages to recognize and phagocytose pathogens, and they activate the classical complement pathway.

Which type of adaptive immune response is most responsible for the clearance of viral infections?

The cell-mediated immune response, specifically CD8+ CTLs.

How do CD8 T cells eliminate infected cells?

CD8 T cells recognize viral peptides presented on MHC molecules on infected host cell surfaces and induce apoptosis in infected cells.

What does it mean that pathogenicity depends on virulence genes?

Pathogenicity depends on virulence genes, not on the bacterial species as a whole; some bacteria can be harmless, but virulence factors can cause disease.

What are toxin genes and how do they affect host cells?

Toxin genes (e.g., exotoxins) directly damage host cells or disturb normal cell signaling, leading to tissue damage or cell death.

How can the effects of toxins be counteracted?

Effects of toxins can be counteracted by neutralizing antibodies and toxin-specific treatments.

What are adhesion genes and their mechanism of action?

Adhesion genes (e.g., pili/fimbrae) allow bacteria to physically attach to host tissues, facilitating colonization.

How can the effects of adhesion be counteracted?

Effects of adhesion can be counteracted by IgA or IgG antibodies that block attachment and promote clearance.

What is immune evasion in bacteria?

Immune evasion involves mechanisms that inhibit immune function, allowing bacteria to survive and replicate in the host.

How can immune evasion be counteracted?

Immune evasion can be counteracted by opsonizing antibodies that bind to surfaces to facilitate recognition and phagocytosis, as well as through vaccines and antimicrobial drugs.