W3 - LINE OF DEFENSES Flashcards by Zari Ami

first line of defenses

SMS RN

skin
mucous membranes
reflexes
normal microbiota

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second line of defenses

PIn2FC

phagocytosis
Inflammation
Interferons
Fever
Complement system

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third line of defense (aquired specfic immunity)

t and b lymphocytes
antibodies

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contains ANTIMICROBIAL peptides
and HIGH AMOUNTS OF SALT that
could cause the bacterial cells to
SHRINK.

sweat

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secreted by SEBACEOUS glands
that contain FATTY ACIDS that kill
some of the microbes such as
GRAM POSITIVE organisms.

sebum

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secreted by different glands in
the body which contain
LYSOZYMES that degrade bacterial
cell walls.

Tears, saliva

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assists in CLEANING and
LUBRICATING the ear, specifically the
ear canal and provides some
protection from bacteria, fungi
and insects.

cerumen/earwax

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prevent proliferation of harmful
microbes in the VAGINA

lactic acid

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induced ACIDITY IN THE STOMACH to
prevent the proliferation of
harmful pathogens

Hydrochloric acid

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Reflexes that prevent entry of
microorganisms into the body
system by flushing out microbes

mechanical
(urination, detection, sneezing, coughing, vomiting)

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Provides innate immunity to viruses or tumor cells

natural killer cells

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NK cells releases ?

perforins and granzyme

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functions to kill the infected cell w viruses or cell that have transformed to become
TUMOR OR CANCER CELLS

perforins and granzyme

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found in epithelium; Acts as ligands for the cell to express a common activating
trigger in the activation of the
receptors found in KAR and KIR

MHC MICA & MHC MICB

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this attachment commans the NK cell not to attack the normal cell

MHC class 1 & KIR

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this attachment trigger NK cells to kill normal cell

KAR & MICA/MICB (stress molecule)

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examine the surface of the
tumor cell in order to determine the levels of MHC class I molecules it has.

Killer Inhibirtory Receptors (KIR)

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CAN KILL THE CELL OR NOT?

“Missing-self” killing

YES

Normal MHC I is missing in the target cell, what remains is the MICA & MICB= KAR is
activated= Killing of the infected cell

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NK cells (Innate immunity)

NK cells -> attachment of KAR & MICA/MICB = kill

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NK cells (adaptive immunity)

NK cells [CD16 receptor] -> bind to FC region of antibody = ADCC

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receptor of NK cells; attach in FC region of antibody

CD16 receptor

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process of NK cells attaching to tail end of antibody

Antibody Dependent Cell-Mediated Cytotoxicity (ADCC)

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an amino acid produced by the PLATELETS during coagulation and directly ANTIBACTERIAL to GRAM POSITIVE bacteria

beta-lysine

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Beta- Lysine acts as _ that damages bacterial cell wall of Gram positive bacteria

cationic detergent

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local response of human tissue to injury

inflammation

purpose of inflammation

LOCALIZE the infection ELIMINATE the cause of injury allow TISSUE REPAIR and healing

Cardinal signs of inflammation

● Rubor - Redness ● Calor- heat ● Tumor- swelling ● Dolor - pain ● Functio laesa - loss of function

capillaru widening/vasodilation =

calor (heat)

Increased capillary permeability =

rubor, tumor

release of fluid and the action of (3) = act on nerves causing DOLOR

histamines prostaglandines bradykinins

Tissue injury can be caused by physical , chemical or pathogenic microorganism .

inflammation

inflammation causes (4)

- vasodilation - increased capillary widening - attraction of WBC - systemic response

causes increase in blood flow and capillaries to leak, releasing phagocytes and clotting factors in the wound

histamine

clotting factor released by histamine; seals the wounded area

platelets

In the presence of injury -> damage cells synthesize = will activate ? and send the sensory stimuli to the brain which will be interpreted as pain

histamine, bradykinin, and prostaglandin; peripheral nerves

process of phagocutes traveling from the BLOOD VESSEL to the TISSUE; refers to the movement of WBCs from the capillaries to the tissue surrounding them via chemotaxis

LEUKOCYTE EXTRAVASATION

more potent mediators that can also cause an increase in blood flow

prostaglandins

the action of histamine + prostaglandin will promote the migration of leukocytes, also know as -

chemotaxis

steps of leukocyte extraversion

CRAD Capture/margination Rolling Adhesion Diapedesis

MARGINATION: WBC expresses ?

L-selectin

MARGINATION: Endothelum expresses ?

E/P-selectin

ADHESION: L-selectin at the surface of the WBC will be replaced by the expression

INTEGRINS

ADHESION: E and P selectin in early phase will be replaced by the expression of

ICAM (Intracellular Adhesion Molecule)

Squeezing through of white blood cells in between endothelial cells

diapedesis

diapedesis is also known as

transmigration

Proteins involved in the four steps of chemotaxis are not encoded by their genes

leukocyte adhesion defect

leukocyte adhesion defect: type 1-> absence of ?

absence of INTEGRIN; affects the Adhesion step of chemotaxis

leukocyte adhesion defect: type 2-> absence of ?

absence of L-SELECTIN; affects the Rolling step of chemotaxis

change in direction of movement of a motile cell in response to a concentration gradient of a specific chemical

Chemotactic response

movement of lymphocytes towards the stimulus

positive chemotaxin

movement of lymphocytes away from the stimulus

negative chemotaxin

= to devour

phagein

= cell

kytos

= process

-osis

phagocytosis is a process by which a cell engulfs a solid particle to form an internal vesicle known as -

phagosome

3 steps of phagocytosis

recognition and adhesion engulfment digestion

Molecules shared by groups of related microbes that are essential for the survival of those organisms and are not found associated with mammalian cells.

Pathogen-Associated Molecular Patters (PAMP)

Structures used by the phagocytes to identify PAMPs; these structures are found on the phagocytes

Pattern Recognition Receptors (PRRs)

pattern recognition receptors (PRRs) which play a crucial role in the initiation of innate immune response by detecting potential harmful pathogens.

Toll-Like receptors

examples of PRRS

lipopeptide receptor flagellin receptor peptidoglycan receptor

TLRs are found on

macrophages dendritic cells epithelial cells

process that allows to kill encapsulated bacteria which are difficult to kill through phagocytosis

opsonization

substances that facilitate opsonization

OPSONINS - IgG - C3B - CRP

PHAGOCYTOSIS PROCESS: Done by forming a MEMBRANE FOLD around a particle or bacteria; Complete closure of the membrane fold will form the phagosome

engulfment

Digestion of microbes is made possible only by the organelle

lysosome

Once the bacterium has already been digested, the residual body/waste product will be released outside the cell through

exocytosis

Failure of the lysosome and phagosome to fuse and form the phagolysosome; Absence of LYST protein

Chediak-Higashi Syndrome

aid in the fusion of lysosome and phagosome to form phagolysosome

Lysosomal Trafficking Proteins (LYST)

functions to transfer melanin from melanocytes to keratinocyes

LYST protein

Absence of LYST =

Albinism

children who have this syndrome will always continue to have RECURRENT BACTERIAL INFECTION because their phagocytes cannot kill the bacteria

Chediak-Higashi Syndrome

Toxic oxygen radicals

SUPEROXIDE HYDROGEN PEROXIDE

reaction of oxygen and NADPh is medaited by ? producing ?

NAPDH oxidase; superoxide

more potent toxic oxygen radical

hydrogen peroxide

Conversion of superoxide to hydrogen peroxide is mediated by the enzyme

superoxide dismutase

aerobic bacteria can protect themselves by breaking down hydrogen peroxide through

catalase

Catalase breaks down hydrogen peroxide into the non-toxic substances

water and oxygen

primary immunodeficiency disorders; ; Characterized by the absence of the phagocyte enzyme NADPH oxidase

CHRONIC GRANULOMATOUS DISEASE

A diverse group of hereditary diseases in which certain cells of the immune system have DIFFICULTY FORMING THE REACTIVE OXYGEN RADICALS that will kill the bacteria

CHRONIC GRANULOMATOUS DISEASE

Group of signaling proteins made and released by host cells in response to the presence of pathogens

interferons

interferons heightens ? and gives and “early warning signal” to the other cells

antiviral defense

interferons is part of what kind of immunity

nonsepcific innate immunity

Mediate the early innate response to viral infection; Have antiviral activities

type I interferon

INTERFERON: Produced by leukocytes/WBC

IFN alpha (IFN-a)

INTERFERON: Produced by fibroblasts

IFN beta (IFN-b)

Decrease viral replication in cells

Type II Interferon

IFN gamma (IFN-y) ALSO KNOWN AS

IMMUNE INTERFERON

No antiviral activities

type 2 interferon

Interferon-gamma is produced by

T delayed hypersensitivity cells

acute phase reactants is synthesizied in

liver

Acts as “temporary antibodies” while antibodies are not yet formed → provide us “temporary protection”

acute phase reactants

Transports iron away from bacteria - Lead to bacterial death

Lactoferrin

Protein that will then neutralize elastase - Might escape from the granules of bacteria upon neutrophil phagocytosis and destroy neighboring tissues

Alpha-1 Antitrypsin

Transports copper away from bacteria

Ceruloplasmin

Prevents loss of iron by urinary excretion - Provide protection to kidney from any form of damage

Haptoglobulin

Forms clots which can trap bacteria - Forms fibrin when activated → produce clots

Fibrinogen

Opsonin - Facilitate the action of phagocytes

CRP (C-reactive Protein)

Fever generating agents

pyrogens

Acts on HYPOTHALAMUS to increase body temp

IL-1

Acts on LIVER to produce acute phase reactants

IL-6

characteristic of adaptive immunity

specificity diversity memory