Immunology Review Notes, Summaries of Immunology

A summary of the immune system: review notes

Typology: Summaries

2021/2022

Uploaded on 08/13/2023

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PHAGOCYTES: “that eats” process of endocytosis
(getting something into their own cytoplasm)
PHAGOCYTOSIS
a. Acute
a. 0-12 hours: time limit wherein our body
should ward off pathogens through the
process of phagocytosis
b. Capability of immune system to ward off
infection.
b. Oxidative burst: Capability of digesting the
organism
c. Exocytosis
a. When respiratory burst happens, it
should have been taken out from the
body (exocytosed)
Free radicals: by product of phagocytosis inside the
body
Excessive phagocytosis = increase free radicals =
Harmful to the body
ANTIOXIDANT: Medications that counter the actions
of free radicals
1. Pathogen ingested should be enclosed in a
VACUOLE.
o PHAGOSOME: Antigen enclosed in a
vacuole (enclosed antigen).
2. Must be infused with lysosome(contains
digestive juices/substances to facilitate
respiratory burst: myeloperoxidase,
peroxidase, protease, transaminase,
lactoferrin, etc.)
o PHAGOLYSOSOME: phagocyte and
lysosome infused with one another
3. When oxidative burst happen,
phagolysosome must be EXOCYTOSED.
Phagocytes: neutrophils, monocytes, macrophage,
eosinophil, dendritic cells (most potent), basophils
IMMUNOCYTES
1. Lymphocytes (reactive cells)
a. T cells
a. During infection, there is a
differentiation of either:
i. T helper: CD4 receptors
ii. T cytotoxic: CD8 receptors
b. B cells
a. Produce/ secrete antibodies
(transmitter of which cells will be
killed)
b. Plasma cells: Activated form
c. NK cells/ assassin cells/ null cells
a. Attack viral infected cells, tumor
cells
b. NO NEED RECEPTORS as they are
capable of releasing perforins
(initiate formation of pores within
the cell leading to cell lysis)
c. Also produce granzymes
T REGULATORY: regulates production and
subsequent reaction
T SUPPRESSOR: counteracts and inhibits the
reaction of T cytotoxic
T DELAYED TYPE HYPERSENSITIVITY:
hypersensitivity reaction
HUMORAL IMMUNITY
Has nothing to do with any type of cells
Consists of:
o Opsonins, antibodies and acute phase
reactants
INNATE vs ADAPTIVE
Innate
Present at brith
Natural, non-specific immunity
Treat all antigens the same
o Homogenous reaction
Lacks memory
Adaptive
Not present at birth
Acquired, specific immunity
Diversed reaction
Has memory
o B memory cells will memorize
infection. They will the DNA of the
antigen
CHECKPOINTS/BARRIERS
1. 1st BARRIER
Skin: LACTIC ACID
Secretions: LYSOZYMES, TRANSFERRIN,
PROTEASES
Cilia linings within the gastrointestinal tract:
facilitates locomotion of microorganisms
Reflexes: sneezing and coughing, prevent
progression to the inner parts of body by
expelling out
Acidity of genitourinary tract and vagina (pH 5):
Lactobacillus acidophilus
o GIT pH 1 (HCl) should be maintained
Normal flora
o Competitive exclusion
2. 2ND BARRIER
Consists of:
o Phagocytes
o Inflammatory/Fever
o Natural antimicrobial substances
Properdins
Complement system
Betalysin
Interferons
Tumor necrotic factor
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PHAGOCYTES: “that eats” – process of endocytosis (getting something into their own cytoplasm)

PHAGOCYTOSIS a. Acute a. 0 - 12 hours : time limit wherein our body should ward off pathogens through the process of phagocytosis b. Capability of immune system to ward off infection. b. Oxidative burst : Capability of digesting the organism c. Exocytosis a. When respiratory burst happens, it should have been taken out from the body (exocytosed) Free radicals: by product of phagocytosis inside the body Excessive phagocytosis = increase free radicals = Harmful to the body ANTIOXIDANT: Medications that counter the actions of free radicals

1. Pathogen ingested should be enclosed in a VACUOLE. o PHAGOSOME: Antigen enclosed in a vacuole (enclosed antigen). 2. Must be infused with lysosome (contains digestive juices/substances to facilitate respiratory burst: myeloperoxidase, peroxidase, protease, transaminase, lactoferrin, etc.) o PHAGOLYSOSOME: phagocyte and lysosome infused with one another 3. When oxidative burst happen, phagolysosome must be EXOCYTOSED. Phagocytes : neutrophils, monocytes, macrophage, eosinophil, dendritic cells (most potent), basophils **IMMUNOCYTES

  1. Lymphocytes (reactive cells) a. T cells** a. During infection, there is a differentiation of either: i. T helper : CD4 receptors ii. T cytotoxic : CD8 receptors b. B cells a. Produce/ secrete antibodies (transmitter of which cells will be killed) b. Plasma cells: Activated form c. NK cells/ assassin cells/ null cells a. Attack viral infected cells, tumor cells b. NO NEED RECEPTORS as they are capable of releasing perforins (initiate formation of pores within the cell leading to cell lysis)

c. Also produce granzymes T REGULATORY: regulates production and subsequent reaction T SUPPRESSOR: counteracts and inhibits the reaction of T cytotoxic T DELAYED TYPE HYPERSENSITIVITY: hypersensitivity reaction HUMORAL IMMUNITY

  • Has nothing to do with any type of cells
  • Consists of: o Opsonins, antibodies and acute phase reactants INNATE vs ADAPTIVE Innate
    • Present at brith
    • Natural, non-specific immunity
    • Treat all antigens the same o Homogenous reaction
    • Lacks memory Adaptive
    • Not present at birth
    • Acquired, specific immunity
    • Diversed reaction
    • Has “memory” o B memory cells will memorize infection. They will the DNA of the antigen **CHECKPOINTS/BARRIERS
  1. 1 st**^ BARRIER
  • Skin : LACTIC ACID
  • Secretions : LYSOZYMES, TRANSFERRIN, PROTEASES
  • Cilia linings within the gastrointestinal tract: facilitates locomotion of microorganisms
  • Reflexes : sneezing and coughing, prevent progression to the inner parts of body by expelling out
  • Acidity of genitourinary tract and vagina (pH 5): Lactobacillus acidophilus o GIT – pH 1 (HCl) should be maintained
  • Normal flora o Competitive exclusion 2. 2 ND^ BARRIER
    • Consists of: o Phagocytes o Inflammatory/Fever o Natural antimicrobial substances ▪ Properdins ▪ Complement system ▪ Betalysin ▪ Interferons ▪ Tumor necrotic factor

3. 3 RD LINE OF DEFENSE

ADAPTIVE IMMUNITY – takes time before it comes into full effect because it is acquired immunity (0- 12 hours infection)

  • After 12hrs - starts adaptive immunity

Specialized cells

  • T cells

• B cells → production of Ab

INFLAMMATORY RESPONSE

  • Cytokines : substances release by cells that uses by the body as a stimulants/messenger. o Most important pro-inflammatory cytokines: **IL- 1 , IL- 6 , TNF-alpha
  1. Acute inflammation**
  • Duration of minutes, hours, or days BUT NOT months or weeks
  • Exudative fluids : leakage of fluid because of inflammation
  • Exudates are greater than transudates

5 CARDINAL SIGNS 1 Redness RUBOR 2 Heat CALOR 3 Swelling TUMOR 4 Pain DALOR 5 Loss of function FUNCTION LAESA

ACUTE → CHRONIC

**1. PERSISTING INFECTION

  1. PROLONGED EXPOSURE
  2. PROGRESSION FROM ACUTE TO CHRONIC
  3. AUTOIMMUNITY** ⎯ systemic lupus erythematosus ⎯ rheumatoid arthritis 2. Chronic inflammation
  • Duration weeks and months
  • 2 resolutions: o Permanent damage or o Complete resolution

ACUTE PHASE REACTANTS (APRs) (+) APR – DECREASE

  • CRP : o Fastest increasing APR in the body o Nonspecific inflammation 1000 times increases
  • Serum Amyloid A (SAA) o Increases 1,000 times but slower
  • Alpha 1 Anti-Trypsin o Alpha globulin that is capable of mopping up the residual of phagocytosis.
  • After phagocytosis, there will be exocytosis. There will be free radicals that will be excreted and protease will be formed that causes damage to the body. o Ex. Elastase – degrading collagen or endothelial lining kaya pag hindi binind

ni antitrypsin madedgrade ang collagen mes. Emphysema : Absence of alpha 1 anti-trypsin (-) APR – INCREASE

  • Prealbumin
  • albumin
  • transferrin Important in inflammation! Ceruloplasmin : binds copper Haptogloblin : binds pre-hemoglobin Kayser fleischer ring : copper deposition in eyes Absence of haptoglobin in inflammation will cause oxidative damage in tissue that is permanent and irreversible Increase of complement system : facilitate lysis of cells
    • Classical
    • Alternative : Factor B
    • Mannose-binding lectin (MBL) o MASP- 1 - Mannan-binding lectin serine protease o MASP- 2