Discuss how Rheumatoid Arthritis is caused when the pathway is inappropriately activated or not functioning properly, provide one other reference than the photo below to expand on how the signaling pathway is disrupted.
Discuss how Rheumatoid Arthritis is caused when the pathway is inappropriately activated or not functioning properly, provide one other reference than the photo below to expand on how the signaling pathway is disrupted.
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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Tumor necrosis factor (TNF) signaling
Discuss how Rheumatoid Arthritis is caused when the pathway is inappropriately activated or not functioning properly, provide one other reference than the photo below to expand on how the signaling pathway is disrupted.
![Blood
TNF-a
IL-17
Int. J. Mol. Sci. 2021, 22, 2719
Keratinocytes
Psoriasis
Th17
IL-17
IL-23
Osteoclasts Synovial fibroblasts.
Joint erosion
TNF-a
Psoriatic arthritis
Macrophages
IL-1, IL-6, TNF-a
Th1
TNF-a
Synovial
fibroblasts
2. TNF-α Signaling in Autoimmune Diseases
2.1. Rheumatoid Arthritis
Osteoclasts
Cathepsins, MMP
Collagen and proteoglycan breakdown
Rheumatoid arthritis
Cartilage and bone destruction
↓
Joint erosion
Figure 2. The role of TNF-α in rheumatoid arthritis (RA) and psoriatic arthritis (PSA). TNF-α is mainly secreted by
macrophage and Th1 cells. In RA, TNF-α activates synovial fibroblasts, which causes the overproduction of cathepsins
and MMP. The breakdown of collagen and proteoglycan follows, resulting in cartilage and bone destruction, as well as
joint erosion. Osteoclasts in RA induce synovial hyperplasia and angiogenesis. In PsA, activated dendritic cells (DCs) and
macrophages secrete TNF-α and IL-23 excessively. IL-23 induces T cells to differentiate in Th17 cells, which secretes IL-17.
IL-17 and TNF-α in the blood activate keratinocytes, resulting in psoriasis (PS). TNF-α also activates osteoclasts, leading to
synovial fibroblast, which results in joint erosion.
4 of 16
Rheumatoid arthritis (RA) is a chronic autoimmune disorder that primarily affects the
joints and typically results in redness, swelling, and arthralgia. In serious cases, it limits the
range of motion [32]. RA affects nearly 1% of the population, and it is characterized by the
inflammation of synovial tissue, leading to progressive damage, including the erosion of
adjacent cartilage and bone, which can lead to chronic disability [33]. TNF-x is considered
the major inflammatory cytokine involved in the pathogenesis of RA and is found in high
frequencies in patients with the disease. Inflammation is associated with the accumulation
of inflammatory cells, predominantly type 1 helper T cells (Th1) and macrophages but
also B cells, plasma cells, and dendritic cells (DCs) [22]. In RA, TNF-α secreted from Th1
cells and macrophages activates synovial fibroblasts, promotes epidermal hyperplasia, and
recruits inflammatory cells [34]. After activation by various cytokines, including IL-1, IL-6,
and TNF-x [35], synovial fibroblasts overexpress cathepsins and matrix metalloproteinases
(MMPs), followed by collagen and proteoglycan breakdown. As a result, cartilage and
bone are destroyed, and finally, joint erosion occurs. Osteoclasts are also important for the
progression of RA pathology throughout TNF-α activation, and activated osteoclasts in RA
induce synovial hyperplasia and angiogenesis (Figure 2) [36].](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2Ff123c09d-ccbd-492d-9b0f-c8892232526f%2Fc2f8c358-3736-4c63-a0cc-cdcf0587c72c%2Fo3p4b9_processed.png&w=3840&q=75)
Transcribed Image Text:Blood
TNF-a
IL-17
Int. J. Mol. Sci. 2021, 22, 2719
Keratinocytes
Psoriasis
Th17
IL-17
IL-23
Osteoclasts Synovial fibroblasts.
Joint erosion
TNF-a
Psoriatic arthritis
Macrophages
IL-1, IL-6, TNF-a
Th1
TNF-a
Synovial
fibroblasts
2. TNF-α Signaling in Autoimmune Diseases
2.1. Rheumatoid Arthritis
Osteoclasts
Cathepsins, MMP
Collagen and proteoglycan breakdown
Rheumatoid arthritis
Cartilage and bone destruction
↓
Joint erosion
Figure 2. The role of TNF-α in rheumatoid arthritis (RA) and psoriatic arthritis (PSA). TNF-α is mainly secreted by
macrophage and Th1 cells. In RA, TNF-α activates synovial fibroblasts, which causes the overproduction of cathepsins
and MMP. The breakdown of collagen and proteoglycan follows, resulting in cartilage and bone destruction, as well as
joint erosion. Osteoclasts in RA induce synovial hyperplasia and angiogenesis. In PsA, activated dendritic cells (DCs) and
macrophages secrete TNF-α and IL-23 excessively. IL-23 induces T cells to differentiate in Th17 cells, which secretes IL-17.
IL-17 and TNF-α in the blood activate keratinocytes, resulting in psoriasis (PS). TNF-α also activates osteoclasts, leading to
synovial fibroblast, which results in joint erosion.
4 of 16
Rheumatoid arthritis (RA) is a chronic autoimmune disorder that primarily affects the
joints and typically results in redness, swelling, and arthralgia. In serious cases, it limits the
range of motion [32]. RA affects nearly 1% of the population, and it is characterized by the
inflammation of synovial tissue, leading to progressive damage, including the erosion of
adjacent cartilage and bone, which can lead to chronic disability [33]. TNF-x is considered
the major inflammatory cytokine involved in the pathogenesis of RA and is found in high
frequencies in patients with the disease. Inflammation is associated with the accumulation
of inflammatory cells, predominantly type 1 helper T cells (Th1) and macrophages but
also B cells, plasma cells, and dendritic cells (DCs) [22]. In RA, TNF-α secreted from Th1
cells and macrophages activates synovial fibroblasts, promotes epidermal hyperplasia, and
recruits inflammatory cells [34]. After activation by various cytokines, including IL-1, IL-6,
and TNF-x [35], synovial fibroblasts overexpress cathepsins and matrix metalloproteinases
(MMPs), followed by collagen and proteoglycan breakdown. As a result, cartilage and
bone are destroyed, and finally, joint erosion occurs. Osteoclasts are also important for the
progression of RA pathology throughout TNF-α activation, and activated osteoclasts in RA
induce synovial hyperplasia and angiogenesis (Figure 2) [36].
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