True or False: FHL patients show increased susceptibility to infection because secretion of IFN-γ in cytotoxic granules is impaired.   True or False: Autoimmune-like symptoms of patients with complement deficiencies are due to the complement pathway’s normal functions in clearing immune complexes from the circulation.

Complement receptors and Fc receptors both contribute to removal of immune complexes from the circulation.  Surprisingly, individuals with defects in the early components of the classical complement cascade (i.e., C1, C2, or C4) suffer from an autoimmune type of kidney damage, rather than from an immunodeficiency leading to increased susceptibility to infections. Why do these complement defects lead to autoimmune kidney damage?

What is the only known effect of deficiencies in complement components C5–C9? Explain this effect.

Correctly order the steps in cellular Immunity. Below is a sequence of events. Place them in the order they should occur, number 1 being the first item. Select the step number from the drop down next to each item. Items to order: a) .Cytotoxic T cell (CTL) recognizes the infected host cell b) The CTL secretes perforin and granzyme, causing apoptosis c) The CTL interacts with epitope presented by MHC-I on the dendritic cell d) The helper T cell activates the CTL cell

List and describe the three outcomes of complement activation.

True/False: Several pathogens produce proteins, either membrane-bound or secreted, that inactivate C3b that might be deposited on the pathogen surface. C3b is specifically targeted due to its central position in all three complement pathways.  Explain.

Describe how phagocytes recognize foreign cells. Explain the mechanism phagocytes use to kill engulfed cells. List some ways pathogens avoid the consequences of phagocytosis. Describe the cause, advantages and disadvantages of fever. Define complement and its role in host defense

Multiple pathways for regulating complement activation limit the potential damage caused by complement deposition on host cells or caused by the spontaneous activation of complement proteins in the plasma. Genetic deficiencies in these mechanisms often lead to chronic inflammatory diseases, but in some cases can paradoxically lead to increased susceptibility to bacterial infections. This latter outcome may occur because: Complement regulatory proteins have dual functions in inhibiting and promoting complement activation. Uncontrolled complement activation leads to the depletion of serum complement proteins. The inhibition of the membrane attack complex by complement regulatory proteins normally leads to enhanced activation of the early steps of the complement pathway. Complement regulatory proteins normally cause the rapid depletion of plasma complement factors. Uncontrolled complement activation recruits the majority of phagocytic cells, leaving few remaining to fight infections in…

What are TLRS? How does this work to ensure to prevent pathogens to cause diseases? Where are the locations of each TLRS? What are they exactly detecting specifically? How are cellular behavior changing after they detect pathogens via TLRS? How does complement get activated? Please explain three pathways of complement activation and end results of complement activation.

Macrophages and neutrophils both contribute to extracellular pathogen protection. Describe their common characteristics, differences in structure and function, and if one were eliminated from the innate immune response, explain which one would be more detrimental to the body and why.