7.1 Cellular Immune Response Part 2

IFN-γ activates macrophages, enhancing their ability to engulf and destroy microbes.

IFN-γ promotes the development of TH1 cells while suppressing the differentiation of TH2 and TH17 cells.

Eosinophils and mast cells are crucial for defending against parasites and allergic reactions, both of which are handled by TH2 cells.

Recombinant IFN-γ is used to treat atopic dermatitis, a skin condition often caused by allergies.

IFN-γ promotes the production of IgG2a antibodies, which are important for fighting infections, and inhibits the production of IgE antibodies, which are associated with allergies.

CD40L-CD40 interaction is a crucial handshake between TH1 cells and macrophages, allowing TH1 cells to activate macrophages for efficient microbe destruction.

IL-4 is the key cytokine responsible for the development of TH2 cells, which primarily combat parasites and allergies.

IL-4, IL-5, and IL-13 are the main cytokines secreted by TH2 cells, orchestrating the immune response against parasites and allergic reactions.

TH2 cells primarily focus on antibody production, with IgE being crucial for fighting parasites.

The TH17 subset is responsible for inducing neutrophil-rich inflammation, a key defense mechanism against fungi and bacteria.

IL-1 and IL-6, both produced in response to bacteria and fungi, play a vital role in triggering the development of TH17 cells.

TH17 cells contribute to combating microbes by producing antimicrobial substances, which directly attack and kill pathogens.

IL-12 and IFN-γ act together to promote the development of TH1 cells, which are crucial for controlling intracellular infections.

TH1 cells activate macrophages to engulf and destroy microbes, a vital defense strategy against intracellular pathogens.

T-bet, STAT1, and STAT4 are essential transcription factors for TH1 cell differentiation, ensuring proper development and function.

TH1 cells are the leading force in phagocyte-mediated host defense, acting as the primary effector cells to control intracellular infections.

TH1 cells are induced by microbes that are engulfed by phagocytes, highlighting their critical role in controlling intracellular pathogens.

Follicular helper T cells play a crucial role in antibody production, providing essential assistance to B cells in generating a diverse repertoire of antibodies.

IFN-γ inhibits the development of both TH2 and TH17 cells, ensuring a balanced immune response based on the specific type of infection.

IFN-γ stimulates the expression of molecules that enhance antigen presentation, making immune cells more efficient in recognizing and mounting an immune response against pathogens.

Eosinophils, a type of white blood cell, play a crucial role in combating parasites and allergic reactions, both of which are primarily handled by TH2 cells.

Recombinant IFN-γ, a lab-made version, is used to treat atopic dermatitis, a skin condition often caused by allergies.

TH1 cells activate macrophages through contact-mediated signals delivered by CD40L-CD40 interactions and through the release of IFN-γ, both contributing to enhanced macrophage function and microbe destruction.

IFN-γ promotes switching to IgG2a, a type of antibody that effectively combats infections, while inhibiting the production of IgE, which is associated with allergies.

TH2 cells primarily stimulate the production of IgE, a type of antibody crucial for combating parasites, and eosinophils, a type of white blood cell also crucial for fighting parasites and allergic reactions.

IL-1, IL-6, and IL-23 are primarily associated with TH17 cells, orchestrating their development and function in combating fungal and bacterial infections.

TH2 cells stimulate alternative macrophage activation, leading to the production of anti-inflammatory molecules that help resolve inflammation and promote tissue repair.

TH17 cells are responsible for inducing neutrophil-rich inflammation, a crucial defense mechanism against fungal and bacterial infections, contributing to the rapid recruitment of neutrophils to the site of infection for effective pathogen clearance.

Pro-inflammatory cytokines like IL-1 and IL-6, produced in response to bacteria and fungi, initiate the differentiation of TH17 cells, setting in motion the immune response against these pathogens.

A key function of TH2 cells is stimulating the production of IgE antibodies and eosinophils, both crucial for combating parasitic infections and allergic reactions.

Upon encountering an infection, CD4+ T cells initially become activated in lymphoid organs, where they encounter antigen-presenting cells carrying fragments of the invading pathogens.

IFN-γ is the primary cytokine responsible for activating macrophages for TH1 cells, leading to enhanced phagocytosis and destruction of microbes, particularly intracellular pathogens.

TH17 cells, a distinct subset of CD4+ T cells, are primarily responsible for inducing neutrophil-rich inflammation, a key defense mechanism against fungal and bacterial infections.

Eosinophils, a type of white blood cell, play a central role in phagocyte-independent defense mediated by the TH2 subset, primarily targeting parasites and allergic reactions.

T-bet, STAT1, and STAT4 are essential transcription factors for TH1 cell differentiation, orchestrating the development of TH1 cells into effective immune responders.

TH1 cells are responsible for activating macrophages to ingest and destroy microbes, particularly those that live inside cells, contributing to the control of intracellular infections.