ch43_immune.pptx

Immune system and

Cell Signaling

Defense against threats

• All ways of rapid dissemination of new phenotypes and rapid evolution.

• Variety of pathogens (viruses, bacteria, protists, worms, arthropods, etc)

• Many pathogens constantly generate variety to change appearance / approach

Retroviruses?

Viruses that work in reverse; take over cells RNA instead of DNA

Bacteria? ways to accomplish rapid

Overview of immune system

a

b

1

2

a

Innate (nonspecific) defenses

• Defend against all pathogens without targeting specific ones

• Faster response

a) External: Creates Barriers

b) Internal: 1) warning other cells

2) attracts attention to site of infection a. inflammation b. complements

3) mounting the attack

a. outside: sending cells out through blood, lymph, interstitial fluid

External defenses

• Skin (physical and chemical barrier)

Sweat contains enzymes and increases salinity

Mucous membranes

• Where skin doesn’t separate internal from external environment

• Ex: eyes, respiratory, digestive, urinary/reproductive tracts

• Defenses: 1) mucus – traps pathogen 2) acidity – denatures proteins

Fig. 43-3

Microbes

PHAGOCYTIC CELL

Vacuole

Internal

innate defenses

• A white blood cell engulfs a microbe, then fuses with a lysosome to destroy the microbe

• Different types of phagocytic cells:

▫ Neutrophils engulf and destroy microbes

▫

Macrophages

▫ Eosinophils discharge enzymes killing parasites

▫

Dendritic cells display foreign

antigens and

initiate acquired

Chemical

Warning signs by infected cells

• Interferons – produced by cells infected by

viruses (only), limits cell to cell spread, and activates macrophages

some are being mass produced with recombinate DNA tech for possible treatment of some cancers

• Defensins - can be secreted by macrophages;

Warning signs by damaged cells

• Inflammatory response – physical damage

causes release of histamine

• Histamine causes local vasodilation – more

Destroying infected cells

• NKC induce apoptosis;

always on patrol

So why don’t they destroy healthy “self” cells?

▫ Normal cells have a class 1 MHC protein on their surface; infected or cancerous cells do not

▫ NKC release a chemical that causes infected cell or cancer

cell start phosphorylation cascade that kills the cell:

Apoptosis: Link to cell cycle

• When normal cells are beyond checkpoint repair they should be eliminated by apoptosis

• Mainly by tumor suppressor gene p53

• Mutations or overexpression can result in cancer: too little cell death

Summary of innate defense

• External – prevent pathogens from getting in

• Internal – identify general pathogen threat,

create warning, attack pathogens, attack infected cells

• Problem: many pathogens have co-evolved to slip by innate defenses or to jump species to species barriers; Emerging Diseases

Overview of immune system

What cells (lymphocytes) make

antigen receptors?

• All lymphocyte

cells made in bone marrow

• T cells – mature in thymus

Acquired Immunity 3

line of defense

• Activated by mainly by dendritic cells that secrete

cytokines (although some macrophages secrete these

chemicals, too)

• Example of cell signaling and communication

• “role of MHC”

Class I MHC: nearly all somatic cells; identify cell as “self”

Class II MHC: Dendritic cells and macrophages

Specific responses: Acquired Immunity

• WBC produced in bone marrow some migrate to thymus to mature into T cells, some stay in bone marrow to mature to B cells

• Can identify a specific marker on pathogen’s surface (MHC)

• Viruses / bacteria / most parasites all have

antigens on cell surface

• Problem: antigens often mutate rapidly

Problem for acquired system (ch. 43.3)

• How can immune system stay current when pathogens are constantly mutating?

B and T cells already have specific 100,000 antigen receptors that recognize epitopes (antigens on pathogen surface)

• Solution:

1) randomly generate receptor shapes that bind with ever changing antigens

2) clonal selection – mass produce the cells with receptors that bind to specific pathogens

Antigen receptor sites on cells MHC:

http://www.hhmi.org/biointeractive/antigen-presentation-and-ctl

read “role of MHC”

Class I MHC: nearly all somatic cells; identify cell as “self”

Random generation of receptor shape(skim over for now)

• Recall introns and exons

• Some introns removed, some introns

randomly left in

Types of T and B cells(beginning of 43.3)

• Helper T cell –

“gets the party started”

• Activated by binding to antigen

presented by macrophage or dendritic cells and/or cytokines

B cells – humoral response

• Produce antibodies – free-floating antigen receptors

https://innovation.org/2017/01/17/building-smart-bombs-attack-c ancer/

• Helper T cells secrete cytokines to activate

B and cytotoxic T cells that have correct

B cells – humoral response

• Antibodies bind to pathogen in bloodstream,

T cells – cell-mediated response

• Cytotoxic T cells (activated by cytokines) – find infected cells presenting antigens

• https://www.hhmi.org/biointeractive/ctl-killing-target-cell

• Destroy infected cell

• Different from NKC

Cytotoxic T Cells: Response to Infected Cells

• Cytotoxic T cells are the effector cells in cell-mediated

immune response

• Cytotoxic T cells make CD8, a surface protein that

greatly enhances interaction between a target cell and a cytotoxic T cell

• Binding to a class I MHC complex on an infected cell

activates a cytotoxic T cell and makes it an active

killer

• The activated cytotoxic T cell secretes proteins that

destroy the infected target cell

Killing action of cytotoxic T’s

• Fig 43.16 Secrete Perforines that cause

apoptosis

When infected cell lyses; pathogens are released and are marked by antibodies

http://www.hhmi.org/biointeractive/cloning-army-t-cells-immune-defense

Finally …

• Memory B and memory T cells

• Survive over long-term to “remember” a pathogen

• Therefore, can quickly clone itself if it binds to returning pathogen creating secondary

Immune system problems

• Transplantation – moving organs to another body

Different surface proteins = invader to be attacked by immune system

Immunosuppressant drug

Immune system disorders. Most are genetic.

Attack on the Immune System: HIV

•

Human immunodeficiency virus (HIV) infects

helper T cells

•

The loss of helper T cells impairs both the

humoral and cell-mediated immune responses

and leads to AIDS

•

HIV eludes the immune system because of

antigenic variation and an ability to remain

latent while integrated into host DNA

HIV

• Breaking into helper T cells specifically to reproduce

• HIV infection AIDS

(Acquired Immune Deficiency Syndrome)

RNA virus or retrovirus. Mutates rapidly, much faster than DNA viruses.

You should now be able to:

1. Distinguish between innate and acquired immunity

2. Name and describe four types of phagocytic cells

3. Describe the inflammation response

4. Distinguish between the following pairs of terms:

antigens and antibodies; B lymphocytes and T lymphocytes; antibodies and B cell receptors;

primary and secondary immune responses; humoral and cell-mediated response; active and passive

immunity

5. Explain how B lymphocytes and T lymphocytes recognize specific antigens

7.

Describe the cellular basis for immunological

memory

8.

Describe the role of MHC in the rejection of

tissue transplants

9.

Describe an allergic reaction, including the

roles of IgE, mast cells, and histamine

10.

Describe some of the mechanisms that