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INF > IMMUNE SYSTEM IN HEALTH AND DISEASE > Flashcards

IMMUNE SYSTEM IN HEALTH AND DISEASE Flashcards

1
Q

WHAT IS INFLAMMATION?

A

A RESPONSE TO INFECTION OR INJURY OF VASCULARISED TISSUES TO ELIMINATE DYING CELLS AND FOREIGN BODIES

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2
Q

CLASSIC SIGNS OF INFLAMMATION?

A
  • HEAT
  • PAIN
  • REDNESS
  • SWELLING
  • LOSS OF FUNCTION
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3
Q

WHICH ENDING IS USED IN NAMES OF INFLAMMATORY DISORDERS?

A

-ITIS

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4
Q

PATHOGENS THAT BECOME TOLERATED BY THE IMMUNE SYSTEM (LIKE THE EPSTEIN BARR VIRUS) ONLY CAUSE ISSUES IN WHICH PEOPLE?

A

IMMUNOCOMPROMISED

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5
Q

WHAT CAUSES INFLAMMATION?

A

INFLAMMATION WAS INITIALLY THOUGHT TO BE DIRECTLY CAUSED BY PATHOGEN BUT IT IS IN FACT A HOST INNATE RESPONSE TO CLEAR INFECTION

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6
Q

WHAT ARE PATHOGEN ASSOCIATED MOLECULAR PATTERNS (PAMPs)?

A
  • MOLECULAR STRUCTURES SHARED BY MICROBES THAT ARE NOT PRESENT ON HOST CELLS
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7
Q

WHAT ARE DAMAGE ASSOCIATED MOLECULAR PATTERNS (DAMPs)?

A
  • STRUCTURES FOUND IN/ON STRESSED, DYING OR DEAD HOST CELLS
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8
Q

GIVE SOME EXAMPLES OF PAMPs (PATHOGEN ASSOCIATED MOLECULAR PATTERNS):

A
  • LIPIDATED OR GLYCOSYLATED MOLECULES (LIPOPROTEINS, LIPOPOLYSACCHARIDES..)
  • ESSENTIAL MICROBIAL PROTEINS (FLAGELLIN, FORMYLATED PEPTIDES..)
  • NUCLEIC ACIDS (DOUBLE STRANDED RNA, UNMETHYLATED CpG DNA..)
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9
Q

HOW CAN BACTERIA AVOID THEIR PAMPs GETTING RECOGNISED AND THEM GETTING DESTROYED?

A
  • BACTERIAL SURFACE IS A POTENT SOURCE OF PAMPs, SO SOME BACTERIA DELIBERATELY MODIFY STRUCTURES TO AVOID BEING RECOGNISED OR CLOAK THEMSELVES IN SELF-PROTEINS (FIBRIN)
  • BACTERIA CAN USE GENETIC VARIATION TO NOT DISPLAY CONSERVED PAMPs THAT COULD BE READILY DETECTED
  • INTRACELLULAR BACTERIA (LIKE M. TUBERCULOSIS) CONTROL PHAGOCYTIC FUNCTION TO LIVE IN MACROPHAGES SO THEY LIVE IN CELLS THAT ARE SUPPOSED TO KILL THEM
  • SOME BACTERIA (LIKE LISTERIA) CO-OPT ACTIN NETWORKS IN HOST CELLS TO LITERALLY PROPEL THEMSELVES OUT OF PHAGOSOMES AND INTO NEIGHBORING CELLS
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10
Q

ARE VIRUSES OR BACTERIA HARDER TO DETECT BY THE IMMUNE SYSTEM?

A

VIRUSES

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11
Q

INNATE RESPONSE TO VIRUSES:

A
  • INNATE RECOGNITION OF VIRAL GENETIC MATERIAL LEADS TO THE PRODUCTION OF INTERFERON (IFN) PROTEINS
  • IFN PROTEINS PUT THE SURROUNDING TISSUE ON A ‘WAR-FOOTING’ TO LIMIT THE SPREAD OF VIRUS
  • THIS CAUSES CELLS TO EXPRESS PROTEINS THAT INHIBIT VIRAL RNA REPLICATION, AND BLOCK PROTEIN SYNTHESIS
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12
Q

WHAT ARE INTERFERON PROTEINS?

A

PROTEINS RELEASED BY HOST CELLS DURING INNATE RESPONSE TO VIRUSES; LEAD UNAFFECTED SURROUNDING CELLS TO PRODUCING PROTEINS THAT INHIBIT VIRAL REPLICATION

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13
Q

WHICH VIRUS TYPE HAS MORE MUTATIONS, DNA OR RNA AND WHY?

A

RNA VIRUSES

THEY REQUIRE REVERSE TRANSCRIPTION WHICH IS INHERENTLY MORE ERROR-PRONE BUT ALLOWS RAPID EVOLUTION OF NEW VARIANTS

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14
Q

WHAT IS ‘ANTIGENIC DRIFT’ IN VIRUSES?

A

POINT AMINO ACID MUTATIONS IN KEY VIRAL PROTEINS

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15
Q

WHAT IS THE DRIVER OF SEASONAL VARIATIONS IN FLU OUTBREAKS?

A

ANTIGENIC DRIFT (POINT AMINO ACID MUTATIONS IN KEY VIRAL PROTEINS)

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16
Q

WHAT ARE THE KEY VIRAL PROTEINS IN INFLUENZA WHICH MUTATE AND PRODUCE SEASONAL VARIATION?

A
  • HAEMAGGLUTININ (H)

- NEURAMIDASE (N)

17
Q

WHAT IS ANTIGENIC SHIFT IN VIRUSES?

A

SIGNIFICANT ALTERATION IN SEQUENCE, OFTEN BY CAPTURING GENETIC SEQUENCES FROM CLOSELY RELATED VIRUSES

  • SUDDEN, RAPID CHANGE
  • SEGMENTED GENOME HELPS THIS A LOT
18
Q

DNA VS RNA VIRUSES, WHICH CAN SUPPORT LARGER GENOMES?

A

DNA

19
Q

% OF THE DNA VIRUS SEQUENCE THAT IS DEDICATED TO IMMUNE EVASION (CONTROLLING THE HOST IMMUNE RESPONSE)?

A

> 50%

20
Q

WHAT IS A LENTIVIRUS?

A

Virus causing chronic and deadly diseases characterized by long incubation periods, in humans and other mammalian species (e.g. HIV)

21
Q

IS HIV RNA OR DNA VIRUS?

A

RNA

22
Q

MAIN CONTRIBUTOR TO HIV-1/AIDS PATHOGENICITY?

A

INDUCTION OF SLOW DECLINE OF HOST CD4+ T CELLS NUMBERS ALLOWING LIFE THREATENING OPPORTUNISTIC INFECTIONS AND CANCERS TO THRIVE

23
Q

WHAT IS AUTOIMMUNITY?

A
  • IMMUNE RESPONSE AGAINST SELF (AUTO) ANTIGEN MISTAKENLY SEEN AS FOREIGN
  • DRIVEN BY IMMUNE RESPONSE TO HOST PEPTIDES THAT BECOMES SELF-REINFORCING!!
  • FAILURE OF TOLERANCE, LEADING TO AN ABERRANT IMMUNE RESPONSE
24
Q

WHAT IS AUTOIMMUNITY?

A
  • IMMUNE RESPONSE AGAINST SELF (AUTO) ANTIGEN MISTAKENLY SEEN AS FOREIGN
  • DRIVEN BY IMMUNE RESPONSE TO HOST PEPTIDES THAT BECOMES SELF-REINFORCING!!
  • FAILURE OF TOLERANCE, LEADING TO AN ABERRANT IMMUNE RESPONSE
25
Q

GENETIC SCREENING FOR AUTOIMMUNE DISEASE?

A
  • MULTIPLE GENES ASSOCIATED (E.G. MHC COMPLEX)
  • EACH GENE INDIVIDUALLY MAKES A SMALL CONTRIBUTION
  • THERE’S LITTLE PREDICTIVE VALUE IN GEN. SCREENING
  • COMPLEX ENVIRONMENT AND GENE INTERACTIONS
  • INITIATING TRIGGERS OFTEN UNKNOWN
26
Q

GENETIC BASIS OF AUTOIMMUNITY/WHAT INITIATES IT?

A
  • STRONG CONSENSUS THAT AUTOIMMUNITY IS INITIATED BY PATHOGENS OR CELLULAR DAMAGE
  • THE IMMUNE RESPONSE TO THIS INSULT ‘CROSS-REACTS’ WITH SELF ANTIGENS THAT THEN DRIVE A SUSTAINED AND CHRONIC RESPONSE TO SELF
  • AUTOIMMUNE RESPONSE IS SELF SUSTAINING
27
Q

MECHANISMS THROUGH WHICH CHRONIC AUTOIMMUNE DISEASE DEVELOPS?

A
  • POSITIVE FEEDBACK FROM INFLAMMATION
  • INABILITY TO CLEAR THE SELF ANTIGEN
  • BROADENING OF THE AUTOIMMUNE RESPONSE
28
Q

EXAMPLE OF HOW PEOPLE CAN BE PREDISPOSED TO AUTOIMMUNITY?

A

CERTAIN MHC (HLA) ALLELES PREDISPOSE PEOPLE TO AUTOIMMUNITY THROUGH THEIR ENHANCED ABILITY TO BIND AND PRESENT SELF-ANTIGEN

29
Q

WHAT IS THE ROLE OF REGULATORY T CELLS?

A

THEY MODULATE THE IMMUNE SYSTEM, MAINTAIN TOLERANCE TO SELF-ANTIGENS AND PREVENT AUTOIMMUNE DISEASE

30
Q

WHAT IS THE FINAL CHECKPOINT THAT STOPS THE INITIATION OF AUTOIMMUNITY?

A

REGULATORY TOLERANCE (REGULATORY T CELLS ENSURING TOLERANCE TO SELF ANTIGENS)

31
Q

CHARACTERISTICS OF TREATMENT FOR AUTOIMMUNITY:

A
  • LIFELONG

- DOESN’T TARGET THE CAUSE, THE AIM IS TO CALM THE IMMUNE SYSTEM DOWN

32
Q

EXAMPLES OF TREATMENTS FOR AUTOIMMUNITY?

A
  • COSTIMULATORY BLOCKADE (TARGETS T CELLS)
  • SMALL MOLECULE DRUGS (CORTICOSTEROIDS, IMMUNOSUPPRESSANTS..)
  • MONOCLONAL ANTIBODIES (ANTI TNF ALPHA, ANTI IL6 AND IL12…)
33
Q

WHAT ARE PRIMARY IMMUNODEFICIENCIES?

A
  • CONGENITAL IMMUNODEFICIENCIES RESULTING FROM GENETIC MUTATIONS
34
Q

IS SECONDARY IMMUNODEFICIENCY PRESENT AT BRITH?

A

NO, IT IS ACQUIRED

35
Q

SEVERE COMBINED IMMUNODEFICIENCIES (SCIDs):

A
  • A RANGE OF VERY SIGNIFICANT PIDs THAT CAUSE DEFECTS IN THE ADAPTIVE IMMUNE RESPONSE
  • EXTREME ILLNESSES
  • PATIENTS OFTEN COME FROM CONSANGUINEOUS FAMILIES (PARENTS WHO ARE CLOSELY RELATED), WHICH HIGHLIGHTS HOW RARE THESE MUTATIONS ARE
36
Q

CASE OF DAVID VETTER:

A
  • BORN WITH A SEVERE COMBINED IMMUNODEFICIENCY (SCID)
  • LIVED FOR 12 YRS
  • SPENT CCA 20 SECONDS OF HIS LIFE IN A NON STERILE ENVIRONMENT
37
Q

WHY CAN NEWBORN SCID PATIENTS APPEAR HEALTHY/ APPEAR TO HAVE GOOD ANTIBODY PRODUCTION?

A

DUE TO MOTHER PROVIDING ANTIBODIES IN PLACENTA AND MILK

38
Q

DESCRIBE TUMOR IMMUNOLOGY:

A
  • TUMORS ARE MADE FROM OUR OWN CELLS, SO THE IMMUNE SYSTEM IS ABLE TO RECOGNISE THEM ONLY TO A CERTAIN EXTENT
  • THE IMMUNE RESPONSE AGAINST TUMOURS IS OFTEN DOMINATED BY REGULATION OR TOLERANCE
  • EVASION OF HOST IMMUNITY IS ONE OF THE HALLMARKS OF CANCER
  • SOME IMMUNE RESPONSES PROMOTE CANCER GROWTH
  • CANCERS CELLS HAVE LOST GENOME INTEGRITY AND ARE CAPABLE OF EVOLVING THEIR TRANSCRIPTOME TO AVOID DETECTION

INF (40 decks)

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