Micro final

M cells

Special cells in the intestines that pass the antigens from the gut to immune cells, helping the body detect invaders in the digestive tract.

Lysozyme scarrs fav

An enzyme found in tears, saliva, and mucus that breaks bacterial cell walls, helping kill bacteria.

Ciliated cells

cells with tiny hair like structures (cilia) that help move mucus trapped in particles out of the respiratory tract (cleaning crew for airway)

Sebum

An oily substance secreted by skin glands that protects and moisturizes the skin and inhibits bacterial growth.

Cytokines

released by innate cells, indicate infection → recruits

Chemokines

early part of infection, recruits to exact location

5 mechanisms of innate immunity

phagocytosis, fever, inflammation, complement, interferon

Phagocytosis

recruitment of phagocytes, cells are engulfed and destroyed by neutrophils, macrophages, and dendritic cells.

fever

systemic rise in body temp (37.8 C or 100.4 F).

Fevers are good bc

Increased speed of reactions (metabolism), force rest, take up iron

Fevers are bad bc

proteins denature, inhibits CNS, causes dehydration

Inflammation

causes vasodilation, increased capillary permeability, increased blood flow = red and warm

Complement

cell lysis, opsonization, inflammation, MAC

MAC

membrane attack complex

Interferon

paul revere - infected cells release IFN, this warns the neighbor cells to be ready for attack and to make AVPs

toll like receptors (TLRs)

receptors that recognize antigens from pathogens and are non-specific. Ex - dsRNA, ss viral RNA, endotoxins (LPS), and flagella are all not in humans

Membranes role in cytolysis

The cell membrane is the direct target during cytolysis. The MAC forms holes in the membranes and compromises its integrity. Loss of membrane function = cell death d/t osmotic lysis.

opsonization

creates handles for phagocytosis either with complement proteins or antibodies

antigen presenting cells

macrophage, B cell, dendritic cell

phagocytic cells

macrophages, neutrophils, dendritic cells

immunoglobulins

antibodies produced by plasma cells

IgG

complement system, opsonization, can cross placenta from mother to fetus

IgA

in colostrum, protects against new bacteria

IgM

The first antibody produced in response to infection, complement system

IgE

activates mast cells and basophils to release histamines → allergic response, inflammation, fights parasites

IgD

B cell receptor

cytotoxic (CD8)

kill infected host cell with MHC1 presentation

helper (CD4)

differentiates into other immune cells

Th1

activates macrophage via MHC2 and turns it into a supermacrophage

Th2

Activates B cell via MHC2, B cell matures into plasma cell (antibodies). More specifically these antibodies are IgE which fight allergens and parasites. There is also mast cells and inflammation.

Th17

recruits neutrophils to the scene

Tfh

Activates B cell via MHC2, B cell matures into plasma cell (antibodies).

T regulatory

Suppresses immune response when done, inhibits dendritic cells (CD4 → MHC2)

Complement triggers

antibodies, endotoxins (LPS)

Complement outcomes

opsonization, inflammation, cytolysis

MHC1

Presented by infected cells, binds to cytotoxic t cells (CD8) and leads to the death of the infected host cell

MHC2

presented by APC cells and binds to helper T cells (CD4)

Natural passive immunity

get from mom

Natural active immunity

get from being sick

Artificial passive immunity

injection, antibody therapy

Artificial active immunity

vaccines

Passive immunity

given antibodies, no memory

Active immunity

making antibodies, yes memory

Live vaccine

weak virus or pathogen used to create immune response, practices all parts of immunity including CD8 cells, long lasting memory (ex - smallpox)

Inactivated vaccine

A virus that has been killed, does not activate CD8 (ex - polio)

Subunit vaccine

inject an antigen for immune response, does not activate CD8 (ex - noravax, HPV)

Toxoid vaccine

inject a toxin to make antibodies just for the toxin, does not activate CD8 (ex - tetanus)

viral vector

piece together a fake virus with DNA for antigen to cause immune response, engages CD8 cells (ex - Johnson & Johnson)

mRNA vaccine

Lipid nanoparticles delivering mRNA for antigen for immune response, engages CD8 cells (ex - maderna, pfizer)

primary response

primary exposure is first exposure to an antigen. Works slow days to weeks, weaker, less antibodies. Memory cells are not present initially. ex - first time getting chicken pox

secondary response

repeated exposure to the same antigen. rapid within hours to days. Stronger, higher antibody levels. Activated from memory B and T cells. ex - getting exposed again or receiving booster shot

Retrovirus

Has and RNA genome, uses reverse transcriptase to turn its RNA into DNA

Infection of CD4 cells

gp120 and gp41 attaches to a receptor om the CD4 cell (coreceptors CCR5 and CXCR4 help). Membrane fusion allows viruses to enter cells. Receptor and coreceptor binds (attachment phase) to HIV glycoprotein = membrane fusion (penetration phase)

Structure of HIV

contains glycoproteins - gp120 and gp41

HIV becomes AIDs when…

CD4 levels are below 200. The immune system weakens and the body becomes vulnerable to opportunistic infections.

Antivirals

Could target reverse transcriptase and integrase process. Some have been successful using protease, which stops budding.

Problem with antivirals

Reverse transcriptase makes a lot of mistakes → evolution = resistance

Solution for the problem with antivirals

More than 1 drug is prescribed at once because it is unlikely to have 3 mutations at the same time