chapter 17: specific/adaptable defenses of the host: the immune response

body defenses innate/ non-specific epithelium, fever, inflammation, complement, interferon, macro/DCs adaptable/ specific “immunity” lymphoid cells humoral non-self Ag Ab & B cells cell-mediated altered self Ag APCs & T cells defense against infection & illness

lymphoid cells: B cells & T cells naïve lymphocytes highly specific (Ag) >10 6 at a time billions made/day live weeks to months

adaptable cells bind Antigen (Ag), not PAMP Ag: bound by WBC receptors BCR TCR Ig/Ab

getting info to lymphocytes naïve B cells and T cells live in lymph nodes, Ag comes to them

lymphoid cell activation: B cells & T cells Ag travels to lymph node alone (B) or attached to APC (B/T) Ag encountered by lymphocyte lymphocyte is activatedlymphocyte clonally expands activated T cells  bloodstream B cell Ab  bloodstream extravasation extravasation at infection site **extravasation video takes about 4 seconds to load**

humoral immunity T cell independent responsehumoral immunity T cell independent response: weak, short,  affinity activation takes several h plasma cells w/in 1 wk memory cells w/in 2 wks

antibodies (Ab) memorymemory acute phaseacute phase

results of Ag-Ab binding

Ab-dependent cell-mediated cytotoxicity (ADCC) Ab-bound target cell lysed by natural killer (NK) cells & eosinophils large parasites are too big for phagocytosis & integument is resistant 1.IgE coats parasites 2.Fc receptor of eosinophil recognizes IgE 3.helminth-bound IgE causes the eosinophil to degranulate (release cytotoxins from granules) NK cells activated by antibodies 1.NK Fc receptor recognizes the Fc portion of Ab bound to target cell 2.NK cell releases cytokines and cytotoxic granules 3.these enter the target cell and trigger apoptosis

chapter 17 learning objectives 1.What kinds of pathogens do the humoral and cell-mediated branches of the immune system target? How do the terms self, non-self and altered-self relate to this discussion? 2.What are the differences between T cells and B cells, in terms of place of maturation and receptors? 3.What is the lymph system? What is the difference between lymph, interstitial fluid and blood? 4.Where are MHC class I, MHC class II, BCRs and TCRs found? 5.In class, we discussed three ways that B cells can be activated and clonally selected. Understand how each of these results in the production of both plasma cells and memory cells. 6.Draw and label the structure of an antibody molecule. Include the following components: light chain, heavy chain, variable region, constant region, disulfide bonds, antigen binding site, and antigen. Compare/contrast IgG and IgM. 7.What five things result from the binding of Ab to Ag? How do the two types of Ab-dependent Cell-mediated cytotoxicity discussed in class differ?

cell-mediated immunity: T cells & APCs Major HistoCompatibility molecules present Ag to TCR MHC Class I on all body cells, MHC Class II only APCs

MHC class I molecules & Cytotoxic T (T c ) cells granzyme production perforin production

MHC class II molecules & Helper T (T H ) cells

T H cell activation of innate cells

T H cell dependent B cell activation

T H activation of CD8 T C cells

T cell activation & memory

the “helper” T cell

lymphocyte response Pathogen group adaptive response Ab (B cell)T C cells (CTLs)T H cells extracellular bacteria bound Ab initiates total immune response* not effective B cell expansion no direct role in elimination intracellular vesicular bacteria internal pathogen renders Ab useless cytosolic replication of bacteria can cause T C response hyperactivation of macrophages* viruses free viruses are bound & neutralized T C cells kill virally- infected cells* activate B cell vs. free viruses & NK cells vs. infected cells no direct role in elimination helminths antibody-mediated cell-dependent cytotoxicity (ADCC)* not effective B cell expansion no direct role in elimination enhance ADCC

comparing the innate & adaptive responses InnateAdaptive phagocytes, NK cells, eosinophils, mast cellsT cells and B cells response present from birthresponse develops in first year of life responds to infection within minutes to hoursresponds to infection after a few days PRRs on phagocytes recognize common pathogen structural patterns BCR & TCRs recognize specific epitope structures all cells of one type have the same receptors each B cell or T cell has a different Ag specificity not clonal– react to common pathogen ligands clonal response by Ag-specific effector T & plasma B cells defense in any connective tissue in bodydefense generated in 2 o lymphoid tissue no memory generatedgenerates memory

coordinated innate & immune attack

coordinated humoral & cell-mediated attack

chapter 17 learning objectives 1.What kind of cells produce MHC class I molecules? Which produce MHC class II? Which T cells interact with these and what does the interaction between T cell and MHC molecule cause? 2.Compare and contrast the Helper T cell and the Cytotoxic T cell (cytotoxic T lymphocyte) 3.How is memory produced in the cell mediated branch of the immune system? 4.Distinguish between the antibody-mediated (humoral) immune system and T cell-mediated immune system. Know the steps and key players in both. 5.Which is the best lymphocyte response for: extracellular bacteria, intracellular vesicular bacteria, viruses and helminths? 6.Compare and contrast innate and adaptable defenses for: response time, specificity, memory, & location of defense. 7.As discussed in class, identify the role of each of the following: lymphoid cell, B cell, T cell, NK cell, eosinophil, dendritic cell, monocyte, and macrophage.