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Renal I > Test 2 (Immune Lecture) > Flashcards

Test 2 (Immune Lecture) Flashcards

1
Q

Causes of Kidney Hypoperfusion

A

1) Intravascular Volume Depletion
2) Reduced Cardiac Output
3) Systemic Vasodilation
4) Renal Vasoconstriction

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2
Q

Pathogenesis of Ischemic AKI

A

1) Epithelial Cell Injury
a) Necrosis
b) Cytoskeleton Disruption

2a) INFLAMMATION:
- White Blood Cell Recruitment along with Neutrophils, Macrophages, Lymphocytes, and DC Cells

2b) ENDOTHELIAL CELL INJURY:
- Activation, Dysfunction, Detachment, Apoptosis, Necrosis

3a) LEUKOCYTE ACTIVATION
- Cytokine Release, Margination,, Tissue Migration, and Reduced Flow

3b) VASOCONSTRICTION
- Cytokine Release, INCR Permeability, INCR Leukocyte Adhesion Molecules, Reuleaux formation, Reduced Flow

4) RESULTS:
- Cellular Shedding
- Cellular Debris
- Loss of Polarity
- Loss of Tight Junctions
- Cytokine Release
- Tubular Obstruction, Backless, TGF-Beta!!!!!!!!!!!!!

5) DEFECTIVE FUNCTION:
- Reduced GFR
- High FENa
- Concentrating Defect

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3
Q

Cell Activation, Injury, and Reduced Microvascular Flow

A

1) Loss of Endothelial Cell to Cell Contacts due to HYPOXIA
2) Expression of Adhesion Molecules
3) Cytokines, Chemokines, and ROS released

Impaired Flow

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4
Q

Sterile Inflammation and DAMPs

A

Sterile Inflammation is induced by Intrinsic DAMAGE- ASSOCIATED MOLECULER PATTERNS (DAMPs):
- Released from dying Parenchymal Cells

  • Generated during Extracellular Matrix remodeling
  • Kidney cells express a subset of TOLL-LIKE RECEPTORS (TLRs)
  • Cells can respond to DAMPs and induce INNATE IMMUNE RESPONSES and subsequent RENAL INFLAMMATION

DAMPs:

1) HMGB1 (Nucleolus)
2) Uric Acid
3) HSPs (Exosomes)—> Renal Tubular Cells
4) HYALURONANS in ECM
5) S100 PROTEIN (Cytoplasm)

  • **DAMPs cause COMPLEMENT ACTIVATION!!!!!!!!
  • CRP helps activate them
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5
Q

Inflammation caused by PAMPs and DAMPs

A 
Innate Immunity (PAMPs):
1) Nucleic Acid: CpG and ds RNA

2) Lipid: Lipid A
3) Protein (PGN)

Homeostatic Inflammation:
1) Nucleic Acid (ATP)

2) Lipid: oxLDL and Saturated Fatty Acids
3) Protein: HSP and HMGB1

  • ***RESULT:
  • Toll Like Receptors
  • NOD like Receptors
  • Protein (PGN)
  • ***ARE ALL ACTIVATED!!!!!!!!

———–>

CAUSE:

  • TNF alpha
  • IL-6
  • IL1 Beta
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6
Q

Ischemia Repercussion Induced TLR-4 Expression in Kidney

A

1) HMGB-1 ECM Components HSPs
2) TLR-4

3) NF-kB!!!!!!! (MyD 88 Dependent/ Independent Pathway)
- major Transcription Factor in promotion for Inflammatory Response

***TLR-4 activation leads to Increased Productions of Proinflammatory Cytokines and Adhesion Molecules, which elicits a strong Inflammatory Response in RENAL TISSUE

  • **Ischmia Repercussion Injury
  • This exacerbates the Kidney Damage already initiated during the Ischemic Phase through MASSIVE LEUKOCYTE INFILTRATION and Cytotoxicities!!!
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7
Q

Complement in AKI, Inflammation, and Fibrosis

A

1) DAMPs
- Classical
- Lectin
- Alternatives

2) C3 and C5 Activation
3) MAC
4) APOPTOSIS
5) Macrophages can cause Inflammatory Cytokines to be produced
6) TGF-Beta is released —–> FIBROSIS!!!!!!

***C3a and C5a promote Inflammatory Cell Recruitment and release of Pro-Inflammatory Cytokines/ Chemokines and REACTIVE OXYGEN SPECIES, thereby intensifying the Immune response and further amplifying the level of tubular Necrosis and Apoptosis

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8
Q

Cell Responses Mediated by DAMPs

A

Renal Cell Necrosis results in Release of DAMPs

Activation of:

1) DENDRITIC CELLS:
- Antigen Presentation
- Migration
- Type I IFNs, CXCL2, IL1Beta, and IL-12
* ACUTE KIDNEY INJURY and INFECTIONS

2) MACROPHAGE:
- ROS, IL1Beta, TNF, IL-6 and Chemokines
* MOST KIDNEY DISEASES*

3) ENDOTHELIAL CELLS:
- TNF, IL-6, Chemokines, and IFN alpha
* IC-GN Diabetes and Sepsis****

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9
Q

Macrophages in Renal Diseases

A

1) M1: (TLR- Ligands, and IFN-alpha)
- Increase TNF-alpha
- Increase IL6
* **AKI!!!!!!

Release:

  • ROS, NO, Lysosomal Enzymes
  • IL1, IL12, IL23, Chemokines

Job:

  • Microbial Actions; Phagocytosis and killing of Bacteria dn Fungi
  • Inflammation

2) M2: (IL13, IL4)
- Increase Arginase-1
- Increase IL10
- Increase MgL-6
* **CKD!!!!!!! (Fibrosis)

Release:

  • IL10 and TGF Beta
  • Proline, Polyamines, TGF-Beta
  • Il4, IL10

Job:

  • Anti Inflammatory Effects
  • Wound Repair, Fibrosis
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10
Q

TH17 Cell

A

1) Activated T Cell —- (IL-23) —->
2) Th17 Cell ——- (IL-17) —–>

3) Tissue Inflammation!!!!!!!
- Leads to recruitment of Neutrophils, Th1, and Monocytes

Cytokines Released:

1) IL-8 (Recruitment of Neutrophils)
2) MCP-1 (Attracts Blood Monocytes)

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11
Q

Role of Treg Cells

A
  • Anti Inflammatory CELLS!!!!!
  • Make sure there is not too much of an Immune Response!!!!!!

Cytokines:

1) IL10
2) TGF-Bets

**Help to GENERATE FIBROBLASTS!!!!!

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12
Q

Host Verses Graft Reponses cause Transplant Rejection

A

1) HISTOCOMPATABILITY AGs are the target for Rejection
2) HYPERACUTE REJECTION is immediate and caused by Antibody
3) ACUTE REJECTION occurs days to weeks after Transplantation and caused by T Cell and maybe Abs
4) CHRONIC REJECTION is seen months or years after transplantation and caused by Vascular Trauma, Inflammatory products of T Cells, Abs

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13
Q

Graft Verses Host Reactions

A

1) DONOR Lymphocytes ATTACK the Graft recipient
2) The Mechanism of GVHD can be ACUTE or CHRONIC

***Successful Organ Transplantion depends on the use of IMMUNOSUPPRESSIVE DRUGS!!!!

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14
Q

Autografts

A
  • Grafts changed from one part to another of the same inidivudal
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15
Q

Isografts

A
  • Grafts exchanged between different individuals of identical genetic Constitutions (Identical Twins)
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16
Q

Allografts (Allogeneic)

A
  • Grafts changed between nonidentical members of the same species (Ex: What happens in Humans)
17
Q

Xenografts (Xenogeneic)

A
  • Graft changed between members of DIFFERENT species
18
Q

Key Concepts

A

1) The condition of the Allograft
2) Donor-Host Antigenic Disparity
3) Strength of Host Anti-Donor Disparity
4) Immunosuppressive Regimen

19
Q

Overview of Immune Events

A

1) APCs trigger CD4+ and CD8+ T Cells
2) Both a LOCAL and SYSTEMIC Immune Response develop
3) Cytokines recruit and activate Immune Cells
4) Development of specific T Cells, NK Cells, or Macrophages (MEDIATED CYTOTOXICITY)
5) Allograft Rejection

20
Q

ABO matching is not Important for:

A

1) Corneal Transplantation
2) Heart Valve Transplantation
3) Bone and Tendon Grafts

21
Q

Blood Group Antigens (ABO)

A

Group AB:

  • No Abs Present
  • A and B Ags Present

Group O:

  • Anti A and B Abs Present
  • No Ags Present

**Abs + Complement = MAC

22
Q

HLA: Matching Donor and Recipient

A
  • The success of Transplantation is dependent on Matching of the MHC Ags
  • These Ags are encoded by the Major Histocompatibility Complex, MHC Class I and Class II
  • In humans, the MHC is termed the Human Leukocyte Antigen Complex, HLA COMPLEX
  • HLA COMPATABILITY between Donor and Recipient is REQUIRED due to the EXTREME POLYMORPHISM of HLA!!!!!!!!!!!!!!!
23
Q

HLA System

A
  • Each individual inherits only 10 to 12 alleles/ person
  • HLA Ags are CO-DOMINANTLY EXPRESSED
  • The CLASS I HLA Ags (HLA-A and HLA-B) are particularly STRONG BARRIERS to TRANSPLANTATION
  • There are thee Most IMPORTANT for transplantation pairs of the CLASS I HLA Ags (HLA-DR, HLA-DP, HLA-DQ) —> Only present on Professional APC

**Lymphocytes LYSIS can be detected by STAINING the CELLS with Acridine Orange, Ethidium Bromide or HEMOTAXIN Stain!!!

24
Q

Microcytotoxicity Test (Class I MHC)

A

1) Add Abs
2) Add Complement to for MAC
3) Add Dye

***If dye accumulates on the Donor Cell and Recipient Cell then the HLA Ags are IDENTICAL!!!!

***If dye accumulates on the Donor Cell but NOT on the Recipient Cell then the HLA Ags are NOT IDENTICAL!!!!

Normally:
- Usually this test is done on a Panel where multiple HLA Ags can be matched. The Mismatches are just as important as the Matches are

25
Q

Microcytotocicity Test for PREFORMED Abs

A

1) Add Patient Serum
2) Add Complement
3) Add Dye

***If Dye accumulates in the Cell then there are PREFORMED Abs PRESENT!!!!

26
Q

Mixed Lymphocyte Response (Class II HLA Typing)

A

1) Add Radiation that is supposed to prevent PROLIFERATION is the Class II MHC are Identical
2) Add Recipient Cells
3) Add H3 Thymidine

***If there is Activation and Proliferation of Recipient cells then the Recipient cells do NOT SHADE Class II MHC of Donor (High Radioactivity Present)

***If there is No Proliferation, and a LOW Amount of Radioactivity, then there is a Class II Match!!!!

27
Q

Host vs Graft Response

A
  • The Immune System attack the DONOR Tissue

0 ADAPTIVE IMMUNE RESPONSE against a Graft

  • This is due to a HIGHER FREQUENCY of T Cells that recognize the Graft as Foreign:
    a) Immunized individuals has
28
Q

Direct vs Indirect Allorecognition

A

Direct:
- T Cell recognizes UNPROCESSED Allogenic MHC Molecules on Graft APCs

Indirect:
- T Cell recognizes PROCESSED peptides on Allogeneic MHC Molecule bound to Self MHC Molecule on Host APC

29
Q

Host vs Graft Response

A
  • Up to 2% of the HOST T CELLS are capable of recognizing and responding to sing FOREIGN MHC
  • NON IMMUNE INJURY of the GRAFT (Danger Signals) activates Endothelial Cells,a dn T Cells enter the Allograft

Effector Mechanisms of Graft Rejection:

1) HUMORAL:
- TH2 (IL4, IL5, IL10)

2) CELLULAR:
- TH1 (IL2, IFN Gamma)

30
Q

Hyperacute Rejection

A
  • Takes Minutes to Hours

- Performed Antidonor Abs and Complement

31
Q

Accelerated Rejection

A
  • Takes Days
  • Reactivation of Sensitized T Cells
  • Complement activation, Endothelial Damage, Inflammation, and Thrombosis
32
Q

Acute Rejection

A
  • Takes Days to Weeks
  • Primary activation of T Cells
  • Activation of CD8+ cells or Abs
33
Q

Chronic Rejection

A
  • Takes Months to Years
  • Both Immunologic and Nonimmunologic Factors
  • Results in OCCLUSION (Ischemia)
34
Q

Mechanism of Rejections

A

1) Hyperacute = HUMORAL
2) Accelerated = HUMORAL

3a) Acute Cellular = CELLULAR (Th1)
3b) Acute Vascular = HUMORAL (Th2)

4) Chronic = HUMORAL

35
Q

Graft vs Host Disease

A
  • Occurs in IMMUNOCOMPROMISED Recipients because their immune system is UNABEL TO REJECT THE ALLOGENEIC CELLS IN THE GRAFT!!!!!
  • Often occurs when transplants are Small Bowel, Lung, or Liver

Acute GVHD: Epithelial Cell Death in Skin, Liver, and GI

Chronic GVHD: Fibrosis and Atrophy of Affected Organs

***Donor APCs can activate Donor CD8+ T Cells by Cross-Presenting recipient Ags on MHC Class I Molecules

Renal I (14 decks)

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