Lecture 8 questions Flashcards
Acute inflammation or injury increases vascular permeability resulting in
redness, edema, and increased gingival crevicular fluid flow
What are the two mechanisms for killing bacteria by neutrophils
oxidative and non-oxidative
what does the oxidative mechanism for killing bacterial involve
reactive oxygen radicals and electron transfer reactions
What does the non-oxidative mechanism for killing bacteria involve
enzymes that cleave
how does a neutrophil protect the host
sends out cytoplasmic projections around bacteria creating a phagolysosome, which when completely surrounding the bacteria, is less damaging for the host
what is the main difference between innate and adaptive/acquired immunity?
innate is based on inherent biological response, while adaptive/acquired is based on recognition of antigens, immune memory and clonal expansion
what are the 3 major cells in chronic periodontitis?
plasma cells > b lymphocytes > t lymphocytes
what do Th1 cells do?
interact with cancer cells or cells that have been infected
what do Th2 cells do
produce antibodies
what do b lymphocytes differentiate into
plasma cells, when acted upon by IL-10
what compounds can serve as antigens?
LPS, bacterial proteins, etc
what can function as antigen presenting cells (APC)
macrophages and langerhans cells
what do the alpha and beta chains in T-cell receptors determine
the type of immune response
what are the cytokines associated with Th1
IL-1, IFN-gamma, TFN-alpha
what are the cytokines associated with Th2
IL-4, IL-5, IL-6, IL-10, IL-13
how are Th1 and Th2 balanced
they are suppressed by IL-10 which has a general anti-inflammatory properties. a lot of IL-10 means that the are is pretty stable
explain the t-cell response
Tc activated by cytokines -> Tc response to intracellular pathogens –> Tc recognize antigen presentation and destroy infected cells
are there many Tc found in periodontitis
no, suggesting that viruses and invasive bacteria are not major players
explain the b-cell response
Ab mediated humoral immunity triggered in response to soluble antigens -> Ag-Ab complex activated complement -> Ag-Ab complex facilitates opsonization -> Th2 activate B cells to plasma cells
what are the 2 types of B cells
conventional: produce Ab against bacteria, they decrease in healthy or treated sites
auto reactive: produce auto-Ab, they don’t decrease after treatment
explain Ab-medidated protection
Ab blocks entry of toxins/viruses (IgM, IgG, IgA) -> immobilizes bacteria (IgM>IgG) –> agglutinates bacteria (IgM, IgG)
explain Ab plus complement-mediated protection
lysing bacteria (IgM, IgG)
explain Ab plus cells-mediated protection
opsonizes bacteria/fungi for phagocytosis (IgG) -> activates extracellular killing (IgG)
what is avidity?
Ag-binding differs among antibody subclasses, not all are capable of effective opsonization or complement activation