specific

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

defense against infection & illness body defenses

innate/

adaptable/

non-specific

specific

epithelium, fever, inflammation, complement, interferon, macro/DCs

“immunity” lymphoid cells

humoral

cell-mediated

non-self Ag

altered self Ag

Ab & B cells

APCs & T cells

lymphoid cells: B cells & T cells

naïve lymphocytes • highly specific (Ag)

• >106 at a time • billions made/day • live weeks to months

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 activated bloodstream

lymphocyte clonally expands activated T cells bloodstream B cell Ab bloodstream extravasation at infection site

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

humoral 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)

memory

acute 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

cell-mediated immunity: Major HistoCompatibility molecules & T cell receptors

CD8 TC cells & MHC Class I molecules ALL body cells

MHC class I molecules & Cytotoxic T (Tc) cells

perforin production

granzyme production

CD4 TH cells & MHC Class II molecules APCs only

TH cell activation by APCs: MHC Class II

T cell memory

the “helper” T cell

lymphocyte response Pathogen group

adaptive response

Ab (B cell)

TC cells (CTLs)

TH 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 TC response

hyperactivation of macrophages*

viruses

free viruses are bound & neutralized

TC cells kill virallyinfected 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 Innate

Adaptive

phagocytes, NK cells, eosinophils, mast cells

T cells and B cells

response present from birth

response develops in first year of life

responds to infection within minutes to hours

responds 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 body

defense generated in 2o lymphoid tissue

no memory generated

generates memory

coordinated innate & immune attack

coordinated humoral & cell-mediated attack

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.

Both macrophages and dendritic cells are members of the innate defenses that routinely phagocytize pathogens. How are they different?

7.

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 and contrast IgG and IgM.

8.

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?

9.

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?

10.

Compare and contrast the Helper T cell and the Cytotoxic T cell (cytotoxic T lymphocyte)

11.

How is memory produced in the cell mediated branch of the immune system?

12.

Distinguish between the antibody-mediated (humoral) immune system and T cell-mediated immune system. Know the steps and key players in both.

13.

Which is the best lymphocyte response for: extracellular bacteria, intracellular vesicular bacteria, viruses and helminths?

14.

Compare and contrast innate and adaptable defenses for: response time, specificity, memory, & location of defense