Humoral Immunity Flashcards
Exam 2
What is considered humoral
macromolecules, found in ‘humors’, antibodies, complement, and can isolate effects from cells
What is humoral immunity (basic terms)
-If you filter cells out, what is left is humoral immunity
What is the first thing that needs to be done in humoral immunity
-first, B-cells must be activated, which can be
-dependent on T-cells (thymus-dependent or TD)
-Independent of T-cells (Thymas independent TI) therefore don’t need T cells
How can thymus independent antigens activate B-cells without T-cell help
-TI-1 antigens
-activate TLR and BCR
-LPS, polymeric carbohydrates
-called mitogens (growth-inducing)
-not species-specific
-high levels of antigen activate many B-cells
What is TI-2 antigens
-need to be polymers
-cross-link BCR’s
-must be mature B-cells
How does cytokines enhance activity even from TI antigens
-B/C bound to antigen AND DC binds same antigen through PRR (can even activate BC more)
What are the benefits of thymus-independent activation
-quick
-great for encapsulated bacteria (TI-2)
-generalist (many species can be targeted)
What is one con of thymus-independent activation
not very specific/ strong
What is linked recognition
when the activating T cells recognize the same antigen as the B-cell
-NOTE they do not recognize the exact same part of the antigen
What makes Thymus-dependent antigens specific/strong
uses linked recognition
What is an example of linked recognition
-hapten-small chemicals that are non-immunogenic alone but when attached to a carrier (usually a protein) become immunogenic
-this is called the hapten carrier effect
-many haptens on same carrier can cross-link BCR’s
What is another reason for the hapten carrier effect
B cells generate Ab against hapten while T cells recognize peptides from carrier protein phagocytosis
Explain how hapten carrier effect, linked recognition, and penicillin allergies all tie together
-many chemicals can spontaneously react with human proteins to form a hapten-carrier complex
-beta-lactams (penicillin), many carriers
-this leads to linked recognition and therefore a strong immune response
How does linked recognition prevent most autoimmunity/preserve self-tolerance
-robust immune response require both (BCR binds of antigen filled by presentation of right peptide and TCR binding the peptide:MHC complex)
-even before that, many other signals are needed to activate the B/T cells
How are antigens presented by macrophages
-opsonized antigens are recognized by complement receptors on subcapsular sinus macrophages
-present antigen to B-cells
-moves antigen to FDC
How are T cell and B cell interactions stabilized
-by SLAM (signaling lymphocyte activation molecules) proteins
-serve to maintain interactions
-also propagates signals
What is the primary focus of B cells after activation
-receive survival and proliferation signals
-divide (apparent after 5 days)
-differentiate
What are germinal centers
-goal: make Ab very fast
-found in follicles
-B cells AND Tfh
-form a dark and light zone
-form later than primary focus
What is the dark zone
-high proliferation and density
-mostly B cells called centroblasts
-low on BCR expression
What is the light zone
-can encounter FDC’s and Tfh
-B cells called centrocytes
-high on BCR expression
What is cyclic reentry
cells can move between the light and dark zone
What does cyclic reentry help with
somatic hypermutations
What is somatic hypermutation
-the fourth source of diversity in Ab
-increase in mutation rate of V-region of Ab
-NOT in C regions (don’t want to hypermutate so it can be recognized)
-accumulate step-wise (if favorable, passed on if not, B cells die)
How does somatic hypermutation happen
-mutations introduced through AID
-clones with higher Ab affinity are selected for
