Systemic lupus erythematosus pathophysiology: Difference between revisions

Jump to navigation Jump to search
← Older editNewer edit →
VisualWikitext
Mmir (talk | contribs)
CMEAdmin, CMEUser, Bureaucrats, bureaucrats, nocaptcha, smwadministrator, Administrators, Widget editors
14,850 edits
Mmir (talk | contribs)
CMEAdmin, CMEUser, Bureaucrats, bureaucrats, nocaptcha, smwadministrator, Administrators, Widget editors
14,850 edits
Line 17: Line 17:


=== Immune abnormalities ===
=== Immune abnormalities ===
Development of systemic lupus erythematosus (SLE) is the due to activation of different mechanisms that may result in [[auto-immune|auto-immunity]]. As a result, body tissues lose their self-tolerance. Affected patients are no longer entirely tolerant to all of their [[Antigens|self-antigens]], consequently progress to an [[Autoimmunity|autoimmune]] disease and develop auto [[antibodies]] as a response. During disease progression, [[B cell|B cells]] and [[Plasma cell|plasma cells]] that make [[Autoantibody|autoantibodies]] are more persistently activated and thus make more [[Autoantibody|autoantibodies]]. These [[autoantibodies]] are targeted predominantly to [[intracellular]] [[nucleoprotein]] particles.<ref name="pmid8519610">{{cite journal |vauthors=Elkon K |title=Autoantibodies in systemic lupus erythematosus |journal=Curr Opin Rheumatol |volume=7 |issue=5 |pages=384–8 |year=1995 |pmid=8519610 |doi= |url=}}</ref>
Development of systemic lupus erythematosus (SLE) is the due to activation of different mechanisms that may result in [[auto-immune|auto-immunity]]. As a result, body tissues lose their self-tolerance. Affected patients are no longer entirely tolerant to all of their [[Antigens|self-antigens]], consequently progress to an [[Autoimmunity|autoimmune]] disease and develop auto [[antibodies]] as a response. During disease progression, [[B cell|B cells]] and [[Plasma cell|plasma cells]] that make [[Autoantibody|autoantibodies]] are more persistently activated and thus make more [[Autoantibody|autoantibodies]]. These [[autoantibodies]] are targeted predominantly to [[intracellular]] [[nucleoprotein]] particles.<ref name="pmid8519610">{{cite journal |vauthors=Elkon K |title=Autoantibodies in systemic lupus erythematosus |journal=Curr Opin Rheumatol |volume=7 |issue=5 |pages=384–8 |year=1995 |pmid=8519610 |doi= |url=}}</ref><ref name="pmid25449682">{{cite journal |vauthors=Yaniv G, Twig G, Shor DB, Furer A, Sherer Y, Mozes O, Komisar O, Slonimsky E, Klang E, Lotan E, Welt M, Marai I, Shina A, Amital H, Shoenfeld Y |title=A volcanic explosion of autoantibodies in systemic lupus erythematosus: a diversity of 180 different antibodies found in SLE patients |journal=Autoimmun Rev |volume=14 |issue=1 |pages=75–9 |year=2015 |pmid=25449682 |doi=10.1016/j.autrev.2014.10.003 |url=}}</ref> This increase in [[autoantibody]] production and persistence is supposed to be [[Downregulate|downregulated]] by anti-idiotypic [[antibodies]] or regulatory immune cells, but the massive [[Immunology|immunologic]] response in SLE prevents this [[downregulation]] to take place. The most important [[immune]] abnormalities that are related to SLE development and progression are: 
<ref name="pmid25449682">{{cite journal |vauthors=Yaniv G, Twig G, Shor DB, Furer A, Sherer Y, Mozes O, Komisar O, Slonimsky E, Klang E, Lotan E, Welt M, Marai I, Shina A, Amital H, Shoenfeld Y |title=A volcanic explosion of autoantibodies in systemic lupus erythematosus: a diversity of 180 different antibodies found in SLE patients |journal=Autoimmun Rev |volume=14 |issue=1 |pages=75–9 |year=2015 |pmid=25449682 |doi=10.1016/j.autrev.2014.10.003 |url=}}</ref>
 
This increase in [[autoantibody]] production and persistence is supposed to be [[Downregulate|downregulated]] by anti-idiotypic [[antibodies]] or regulatory immune cells, but the massive [[Immunology|immunologic]] response in SLE prevents this [[downregulation]] to take place. 
 
The most important [[immune]] abnormalities that are related to SLE development and progression are: 
==== Signaling abnormalities ====
* Increase in circulating [[plasma cells]] and [[Memory B cell|memory B cells]] that is associated with SLE activity
* Protein kinases are responsible for intracellular cytokine signal. Intracellular signaling is leading to various types of cell response, such as:
* Decrease in [[cytotoxic T cells]], decrease in [[suppressor T cells|suppressor T cell]]'s function, and impaired generation of [[T-cell|polyclonal T-cell]] cytolytic activity
** Cell migration
* Increased number and activity of [[T helper cell|helper T cells]]
** Cell proliferation
* [[Polyclonal antibody|Polyclonal]] activation of [[B cell|B cells]] and abnormal [[B-cell receptor]] signaling
** Inflammatory response
* Increase in [[B cell|B cells]] life span
* Cell signaling abnormalities will lead to:
* Signaling abnormalities of T and B [[Lymphocyte|lymphocytes]], which include:
** T and B [[Lymphocyte|lymphocytes]] cellular hyperactivity
** Cellular hyperactivity
** T and B [[Lymphocyte|lymphocytes]] hyper responsiveness
** Hyper responsiveness
** Persistence of autoreactive T cells that would otherwise have been deleted
* Increased expression of [[interferon alpha]] (IFN-α) inducible [[RNA]] transcripts by [[Mononuclear cells|mononuclear]] cells leads to elevated levels of [[IFN-α]].<ref name="pmid15593221">{{cite journal |vauthors=Kirou KA, Lee C, George S, Louca K, Papagiannis IG, Peterson MG, Ly N, Woodward RN, Fry KE, Lau AY, Prentice JG, Wohlgemuth JG, Crow MK |title=Coordinate overexpression of interferon-alpha-induced genes in systemic lupus erythematosus |journal=Arthritis Rheum. |volume=50 |issue=12 |pages=3958–67 |year=2004 |pmid=15593221 |doi=10.1002/art.20798 |url=}}</ref> Increased availability of stimulatory [[nucleic acids]] would implicate [[Interferon type I|IFN-I]] production, that is responsible for [[chronic]] and recurrent characteristics of the SLE.
* Signaling abnormalities of T and B [[Lymphocyte|lymphocytes]], may be due to:
* Increased expression of specific [[Genetic|genetic factors]] that may be associated with promoting [[autoimmunity]]
* Dysfunctional signaling in [[T-Cells|T]] and [[B cell|B cells]] that may be due to:
** Increased [[calcium]] responses to [[antigen]] stimulation
** Increased [[calcium]] responses to [[antigen]] stimulation
** [[Hyperphosphorylation]] of [[cytosolic]] [[protein]] substrates
** [[Hyperphosphorylation]] of [[cytosolic]] [[protein]] substrates
** Decreased nuclear factor kB
** Decreased nuclear factor kB
** Abnormal [[Potassium channels|voltage-gated potassium channels]], these channels facilitate excessive [[calcium]] entry into [[T cells]]
** Abnormal [[Potassium channels|voltage-gated potassium channels]], these channels facilitate excessive [[calcium]] entry into [[T cells]]
* Increased level of microparticles (MPs):
 
** Microparticles are small, membrane-bound vesicles enclose [[DNA]], [[RNA]], [[nuclear]] proteins, [[cell adhesion molecule]]<nowiki/>s, [[Growth factor|growth factors]], and [[Cytokine|cytokines]]
==== General ====
** They are shed from cells during [[apoptosis]] or activation
* Increased expression of specific [[Genetic|genetic factors]] that may be associated with promoting [[autoimmunity]]
** Microparticles can drive [[inflammation]] and [[autoimmunity]] by their derivatives<ref name="pmid23672591">{{cite journal |vauthors=Dye JR, Ullal AJ, Pisetsky DS |title=The role of microparticles in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus |journal=Scand. J. Immunol. |volume=78 |issue=2 |pages=140–8 |year=2013 |pmid=23672591 |doi=10.1111/sji.12068 |url=}}</ref>
* Increased expression of [[interferon alpha]] (IFN-α) inducible [[RNA]] transcripts by [[Mononuclear cells|mononuclear]] cells leads to elevated levels of [[IFN-α]].<ref name="pmid15593221">{{cite journal |vauthors=Kirou KA, Lee C, George S, Louca K, Papagiannis IG, Peterson MG, Ly N, Woodward RN, Fry KE, Lau AY, Prentice JG, Wohlgemuth JG, Crow MK |title=Coordinate overexpression of interferon-alpha-induced genes in systemic lupus erythematosus |journal=Arthritis Rheum. |volume=50 |issue=12 |pages=3958–67 |year=2004 |pmid=15593221 |doi=10.1002/art.20798 |url=}}</ref> Increased availability of stimulatory [[nucleic acids]] would implicate [[Interferon type I|IFN-I]] production, that is responsible for [[chronic]] and recurrent characteristics of the SLE.
* Elevated levels of circulating [[TNF-alpha]] correlate with active disease, and [[TNF]] is expressed in [[Kidney|renal tissue]] in [[lupus nephritis]]
* Elevated levels of circulating [[TNF-alpha]] correlate with active disease, and [[TNF]] is expressed in [[Kidney|renal tissue]] in [[lupus nephritis]]
* Abnormally high levels of [[CD4]] on [[erythrocytes]] (E-CD4) and low levels of erythrocyte complement receptor type one (E-CR1) are characteristic of SLE, and combined measurement of the 2 molecules has high diagnostic sensitivity and specificity for lupus
* Abnormally high levels of [[CD4]] on [[erythrocytes]] (E-CD4) and low levels of erythrocyte complement receptor type one (E-CR1) are characteristic of SLE, and combined measurement of the 2 molecules has high diagnostic sensitivity and specificity for lupus
* Increased number of circulating [[neutrophils]] undergoing NETosis (NET=[[neutrophil extracellular traps]]), a form of [[apoptosis]] specific for [[Neutrophil|neutrophils]], releases [[DNA]] bound to [[protein]] in protein nets, which stimulates anti-DNA and [[Interferon-alpha|IFN-alpha]] production
 
* Increased [[neutrophil]] extracellular trap leads to: <ref name="pmid26658004">{{cite journal |vauthors=Barnado A, Crofford LJ, Oates JC |title=At the Bedside: Neutrophil extracellular traps (NETs) as targets for biomarkers and therapies in autoimmune diseases |journal=J. Leukoc. Biol. |volume=99 |issue=2 |pages=265–78 |year=2016 |pmid=26658004 |doi=10.1189/jlb.5BT0615-234R |url=}}</ref>
==== Neutrophil ====
*Increased number of circulating [[neutrophils]] undergoing NETosis (NET=[[neutrophil extracellular traps]]), a form of [[apoptosis]] specific for [[Neutrophil|neutrophils]], releases [[DNA]] bound to [[protein]] in protein nets, which stimulates anti-DNA and [[Interferon-alpha|IFN-alpha]] production
*Increased [[neutrophil]] extracellular trap leads to: <ref name="pmid26658004">{{cite journal |vauthors=Barnado A, Crofford LJ, Oates JC |title=At the Bedside: Neutrophil extracellular traps (NETs) as targets for biomarkers and therapies in autoimmune diseases |journal=J. Leukoc. Biol. |volume=99 |issue=2 |pages=265–78 |year=2016 |pmid=26658004 |doi=10.1189/jlb.5BT0615-234R |url=}}</ref>
** [[thrombus]] formation
** [[thrombus]] formation
** Increased disease activity and [[Lupus nephritis|renal disease]] and thus can be used even as a disease activity marker
** Increased disease activity and [[Lupus nephritis|renal disease]] and thus can be used even as a disease activity marker
** [[endothelial cells|Endothelial cell]] damage and [[inflammation]] in [[Atherosclerosis|atherosclerotic]] [[plaques]], which may contribute to accelerated [[atherosclerosis]] in systemic lupus erythematosus
** [[endothelial cells|Endothelial cell]] damage and [[inflammation]] in [[Atherosclerosis|atherosclerotic]] [[plaques]], which may contribute to accelerated [[atherosclerosis]] in systemic lupus erythematosus
==== Microparticles ====
*Increased level of microparticles (MPs):
** Microparticles are small, membrane-bound vesicles enclose [[DNA]], [[RNA]], [[nuclear]] proteins, [[cell adhesion molecule]]<nowiki/>s, [[Growth factor|growth factors]], and [[Cytokine|cytokines]]
** They are shed from cells during [[apoptosis]] or activation
** Microparticles can drive [[inflammation]] and [[autoimmunity]] by their derivatives<ref name="pmid23672591">{{cite journal |vauthors=Dye JR, Ullal AJ, Pisetsky DS |title=The role of microparticles in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus |journal=Scand. J. Immunol. |volume=78 |issue=2 |pages=140–8 |year=2013 |pmid=23672591 |doi=10.1111/sji.12068 |url=}}</ref>
==== B-Cell related ====
* Increase in circulating [[plasma cells]] and [[Memory B cell|memory B cells]] that is associated with SLE activity
* [[Polyclonal antibody|Polyclonal]] activation of [[B cell|B cells]] and abnormal [[B-cell receptor]] signaling
* Increase in [[B cell|B cells]] life span
==== T-Cell related ====
<div style="-webkit-user-select: none;">
* Decrease in [[cytotoxic T cells]], decrease in [[suppressor T cells|suppressor T cell]]'s function, and impaired generation of [[T-cell|polyclonal T-cell]] cytolytic activity
* Increased number and activity of [[T helper cell|helper T cells]]
*


* As an example of immune abnormalities and their complications, nervous system involvement in SLE is due to:
* As an example of immune abnormalities and their complications, nervous system involvement in SLE is due to:
Line 86: Line 104:
** It can also interfere with [[antigen processing]] by activation of [[macrophages]] and hence increase the degree of [[autoimmunity]].
** It can also interfere with [[antigen processing]] by activation of [[macrophages]] and hence increase the degree of [[autoimmunity]].


=== Lupus nephritis ===
In the initial phase of the disease, the immune deposits and/or autoantibodies induce cytokine production in renal resident cells, leading to further inflammatory cytokine/chemokine expression and leukocyte infiltration and activation. Then, infiltrate leukocytes, such as macrophages (M''φ'') and dendritic cells (DCs), secrete a variety of cytokines and activate naïve T cells, leading the cytokine profile towards T helper (Th)1, Th2, and/or Th17.<div style="-webkit-user-select: none;">
==Genetics==
==Genetics==
Systemic lupus erythematosus is transmitted in [[polygenic inheritance]] pattern. [[Genes]] involved in the [[pathogenesis]] of systemic lupus erythematosus include [[HLA]] class [[polymorphism]], [[complement system]] related [[genes]], and other genes related to [[Immune systems|immunologic system]] as well.
Systemic lupus erythematosus is transmitted in [[polygenic inheritance]] pattern. [[Genes]] involved in the [[pathogenesis]] of systemic lupus erythematosus include [[HLA]] class [[polymorphism]], [[complement system]] related [[genes]], and other genes related to [[Immune systems|immunologic system]] as well.
Line 96: Line 117:
!Gene class
!Gene class
! colspan="1" rowspan="1" |Gene subtype
! colspan="1" rowspan="1" |Gene subtype
!
|-
|-
!HLA  
!HLA  
| colspan="1" rowspan="1" |DR2, DR3, DR4, DR7, DR8, DRw12, DQw2, DQA1,
| colspan="1" rowspan="1" |DR2, DR3, DR4, DR7, DR8, DRw12, DQw2, DQA1,
DQB1, DQ6, DQw6, DQ7, DQw7, DQw8, DQw9, B61, B8
DQB1, DQ6, DQw6, DQ7, DQw7, DQw8, DQw9, B61, B8
|HLA-DR2 and HLA-DR3 confer an overall 2-to-3-fold increased risk for SLE
''HLA-DQ'' and –''DR'' alleles show strong associations with SLE autoantibodies
|-  
|-  
!Non-HLA   
!Non-HLA   
Line 122: Line 146:


Humhr 3005  
Humhr 3005  
|
|-  
|-  
!Complement System  
!Complement System  
| colspan="1" rowspan="1" |C2, C4, C1q  
| colspan="1" rowspan="1" |C2, C4, C1q  
|
|}
|}


Revision as of 19:08, 27 July 2017

https://https://www.youtube.com/watch?v=0junqD4BLH4&wmode=transparent%7C350}}

Systemic lupus erythematosus Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Systemic lupus erythematosus from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Criteria

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X Ray

CT

MRI

Echocardiography or Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Lupus and Quality of Life

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Systemic lupus erythematosus pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Systemic lupus erythematosus pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

National Guidelines Clearinghouse

NICE Guidance

FDA on Systemic lupus erythematosus pathophysiology

on Systemic lupus erythematosus pathophysiology

Systemic lupus erythematosus pathophysiology in the news

Blogs onSystemic lupus erythematosus pathophysiology

Directions to Hospitals Treating Systemic lupus erythematosus

Risk calculators and risk factors for Systemic lupus erythematosus pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mahshid Mir, M.D. [2] Cafer Zorkun, M.D., Ph.D. [3] Raviteja Guddeti, M.B.B.S. [4]

Overview

The pathophysiology of systemic lupus erythematosus involves the immune system. There are other factors like genetic factors, hormonal abnormalities, and environmental factors that play some roles as well. The most prominent events involving immune abnormalities are related to persistent activation of B cells and plasma cells that make auto-antibodies during disease progression. The most prominent events involving hormonal abnormalities are due to prolactin and estrogen. The most important environmental factors related to disease progression are ultraviolet (UV) light and some infections. On microscopic histopathological analysis, apoptotic keratinocytes, vacuolization of the basement membrane, and dermal mucin deposition are characteristic findings of SLE dermatitis, and active or inactive endocapillary or extracapillary segmental glomerulonephritis are characteristic findings of SLE nephritis.

Pathogenesis

The progression of systemic lupus erythematosus (SLE) involves the immune system. Nearly all of the pathological manifestation of SLE are due to antibody formation and the creation and deposition of immune complexes in different organs of the body. When the immune complexes are formed, they will deposit in different body tissues and vessels, which may lead to complement activation and more organ damage. There are other factors like genetic factors, hormonal abnormalities, and environmental factors that play some roles as well.

Immune abnormalities

Development of systemic lupus erythematosus (SLE) is the due to activation of different mechanisms that may result in auto-immunity. As a result, body tissues lose their self-tolerance. Affected patients are no longer entirely tolerant to all of their self-antigens, consequently progress to an autoimmune disease and develop auto antibodies as a response. During disease progression, B cells and plasma cells that make autoantibodies are more persistently activated and thus make more autoantibodies. These autoantibodies are targeted predominantly to intracellular nucleoprotein particles.[1][2] This increase in autoantibody production and persistence is supposed to be downregulated by anti-idiotypic antibodies or regulatory immune cells, but the massive immunologic response in SLE prevents this downregulation to take place. The most important immune abnormalities that are related to SLE development and progression are: 


Signaling abnormalities

  • Protein kinases are responsible for intracellular cytokine signal. Intracellular signaling is leading to various types of cell response, such as:
    • Cell migration
    • Cell proliferation
    • Inflammatory response
  • Cell signaling abnormalities will lead to:
    • T and B lymphocytes cellular hyperactivity
    • T and B lymphocytes hyper responsiveness
    • Persistence of autoreactive T cells that would otherwise have been deleted
  • Signaling abnormalities of T and B lymphocytes, may be due to:

General

  • Increased expression of specific genetic factors that may be associated with promoting autoimmunity
  • Increased expression of interferon alpha (IFN-α) inducible RNA transcripts by mononuclear cells leads to elevated levels of IFN-α.[3] Increased availability of stimulatory nucleic acids would implicate IFN-I production, that is responsible for chronic and recurrent characteristics of the SLE.
  • Elevated levels of circulating TNF-alpha correlate with active disease, and TNF is expressed in renal tissue in lupus nephritis
  • Abnormally high levels of CD4 on erythrocytes (E-CD4) and low levels of erythrocyte complement receptor type one (E-CR1) are characteristic of SLE, and combined measurement of the 2 molecules has high diagnostic sensitivity and specificity for lupus

Neutrophil

Microparticles

B-Cell related

T-Cell related


Hormonal abnormalities

The following evidence is suggestive of the hormonal predisposition to SLE:

Hormones that are related to disease progression:[7]

Environmental factors


Lupus nephritis

In the initial phase of the disease, the immune deposits and/or autoantibodies induce cytokine production in renal resident cells, leading to further inflammatory cytokine/chemokine expression and leukocyte infiltration and activation. Then, infiltrate leukocytes, such as macrophages (Mφ) and dendritic cells (DCs), secrete a variety of cytokines and activate naïve T cells, leading the cytokine profile towards T helper (Th)1, Th2, and/or Th17.

Genetics

Systemic lupus erythematosus is transmitted in polygenic inheritance pattern. Genes involved in the pathogenesis of systemic lupus erythematosus include HLA class polymorphism, complement system related genes, and other genes related to immunologic system as well.

The following evidence is also suggestive of the genetic predisposition of SLE:[10]

  • Increase of disease occurrence in identical twins
  • Increased disease frequency among first degree relatives
  • The increased risk of developing the disease in siblings of SLE patients
Gene class Gene subtype
HLA DR2, DR3, DR4, DR7, DR8, DRw12, DQw2, DQA1,

DQB1, DQ6, DQw6, DQ7, DQw7, DQw8, DQw9, B61, B8

HLA-DR2 and HLA-DR3 confer an overall 2-to-3-fold increased risk for SLE

HLA-DQ and –DR alleles show strong associations with SLE autoantibodies

Non-HLA Mannose binding lectin polymorphisms

Tumour necrosis factor α

T cell receptor

Interleukin 6

CR1

Immunoglobulin Gm and Km

FcγRIIA (IgG Fc receptor)

FcγRIIIA (IgG Fc receptor)

PARP (poly-ADP ribose polymerase)

Heat shock protein 70

Humhr 3005

Complement System C2, C4, C1q

Associated Conditions

Gross Pathology

On gross pathology of kidney, bilateral pallor, and hypertrophy of kidneys are characteristic findings of systemic lupus erythematosus.

On gross pathology of brain, infarct regions and hemorrhages are characteristic findings of systemic lupus erythematosus.

On gross pathology of cardiac valves, cardiomegaly and valvular vegetation are characteristic findings of systemic lupus erythematosus.

On gross pathology of pleura, pleuritis and pleural fibrosis are characteristic findings of systemic lupus erythematosus.

Microscopic Pathology

On microscopic histopathological analysis, apoptotic keratinocytes, vacuolization of the basement membrane, and dermal mucin deposition are characteristic findings of SLE dermatitis, and active or inactive endocapillary or extracapillary segmental glomerulonephritis are characteristic findings of SLE nephritis.

Skin involvement histopathology:

Common shared histopathologic features among all different subtypes of cutaneous lupus include:

SLE dermatitis subtype Specific microscopic findings
Acute cutaneous lupus erythematosus
Subacute cutaneous lupus erythematosus
Chronic cutaneous lupus erythematosus

Glomerulonephritis histopathology:

Class SLE nephritis subtype Light microscopy findings Electron microscopy/Immunofluorescence findings
I Minimal mesangial lupus nephritis -
II Mesangial proliferative lupus nephritis
III Focal lupus nephritis
IV Diffuse lupus nephritis
  • Subendothelial deposits specially during the active phase
  • Diffuse wire loop deposits with little or no glomerular proliferation
V Lupus membranous nephropathy
VI Advanced sclerosing lupus nephritis

Synovial involvement histopathology

Mucosal involvement histopathology


Videos

{{#ev:youtube|Tw07BFaDEo0}}

References

  1. ↑ Elkon K (1995). "Autoantibodies in systemic lupus erythematosus". Curr Opin Rheumatol. 7 (5): 384–8. PMID 8519610.
  2. ↑ Yaniv G, Twig G, Shor DB, Furer A, Sherer Y, Mozes O, Komisar O, Slonimsky E, Klang E, Lotan E, Welt M, Marai I, Shina A, Amital H, Shoenfeld Y (2015). "A volcanic explosion of autoantibodies in systemic lupus erythematosus: a diversity of 180 different antibodies found in SLE patients". Autoimmun Rev. 14 (1): 75–9. doi:10.1016/j.autrev.2014.10.003. PMID 25449682.
  3. ↑ Kirou KA, Lee C, George S, Louca K, Papagiannis IG, Peterson MG, Ly N, Woodward RN, Fry KE, Lau AY, Prentice JG, Wohlgemuth JG, Crow MK (2004). "Coordinate overexpression of interferon-alpha-induced genes in systemic lupus erythematosus". Arthritis Rheum. 50 (12): 3958–67. doi:10.1002/art.20798. PMID 15593221.
  4. ↑ Barnado A, Crofford LJ, Oates JC (2016). "At the Bedside: Neutrophil extracellular traps (NETs) as targets for biomarkers and therapies in autoimmune diseases". J. Leukoc. Biol. 99 (2): 265–78. doi:10.1189/jlb.5BT0615-234R. PMID 26658004.
  5. ↑ Dye JR, Ullal AJ, Pisetsky DS (2013). "The role of microparticles in the pathogenesis of rheumatoid arthritis and systemic lupus erythematosus". Scand. J. Immunol. 78 (2): 140–8. doi:10.1111/sji.12068. PMID 23672591.
  6. ↑ Costenbader KH, Feskanich D, Stampfer MJ, Karlson EW (2007). "Reproductive and menopausal factors and risk of systemic lupus erythematosus in women". Arthritis Rheum. 56 (4): 1251–62. doi:10.1002/art.22510. PMID 17393454.
  7. ↑ 7.0 7.1 Lahita RG (1999). "The role of sex hormones in systemic lupus erythematosus". Curr Opin Rheumatol. 11 (5): 352–6. PMID 10503654.
  8. ↑ Hughes GC, Choubey D (2014). "Modulation of autoimmune rheumatic diseases by oestrogen and progesterone". Nat Rev Rheumatol. 10 (12): 740–51. doi:10.1038/nrrheum.2014.144. PMID 25155581.
  9. ↑ Cohen-Solal JF, Jeganathan V, Grimaldi CM, Peeva E, Diamond B (2006). "Sex hormones and SLE: influencing the fate of autoreactive B cells". Curr. Top. Microbiol. Immunol. 305: 67–88. PMID 16724801.
  10. ↑ Sullivan KE (2000). "Genetics of systemic lupus erythematosus. Clinical implications". Rheum. Dis. Clin. North Am. 26 (2): 229–56, v–vi. PMID 10768211.
  11. ↑ Petry F, Botto M, Holtappels R, Walport MJ, Loos M (2001). "Reconstitution of the complement function in C1q-deficient (C1qa-/-) mice with wild-type bone marrow cells". J. Immunol. 167 (7): 4033–7. PMID 11564823.
  12. ↑ Li R, Peng H, Chen GM, Feng CC, Zhang YJ, Wen PF, Qiu LJ, Leng RX, Pan HF, Ye DQ (2014). "Association of FCGR2A-R/H131 polymorphism with susceptibility to systemic lupus erythematosus among Asian population: a meta-analysis of 20 studies". Arch. Dermatol. Res. 306 (9): 781–91. doi:10.1007/s00403-014-1483-5. PMID 24997134.
  13. ↑ Sepehr A, Wenson S, Tahan SR (2010). "Histopathologic manifestations of systemic diseases: the example of cutaneous lupus erythematosus". J. Cutan. Pathol. 37 Suppl 1: 112–24. doi:10.1111/j.1600-0560.2010.01510.x. PMID 20482683.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Systemic_lupus_erythematosus_pathophysiology&oldid=1331526"