# IMMUNOBIOLOGY OF CHONDROCYTES

> **NIH NIH R01** · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · 1989 · $115,133

## Abstract

Immunopathological events are thought to result in the initiation and
progressive destruction of joints in diseases like rheumatoid arthritis.
The hallmark of disease consists of progressive erosion of articular
cartilage by proliferating synovial tissue.  The characteristic of pannus
and the inflamed synovium is unregulated growth.  This tissue consists of
synovial fibroblasts with infiltration of mononuclear phagocytes and
lymphocytes.  Normally pannus maintains a gradient of movement towards
which this tissue destruction is directed and this gradient is provided by
articular cartilage.  This is based on two clinical observations, namely if
cartilage is completely destroyed or removed by surgical means such as in
arthoplasty, it results in loss of gradient and quiescence of
inflammation.  This suggests that cartilage may provide an immune stimulus
for inflammation.  Previous workers have directed their attention to type
II collagen which is uniquely found in the matrix of articular cartilage.
We have directed our investigations to the cellular component of articular
cartilage, namely, chondrocytes.  This approach has led us to the discovery
of la antigen expression on articular chondrocytes.  These cells not only
express la antigen but perform a number of la mediated immune functions
such as presenting antigen and inducing allogeneic and autologous
lymphocyte reaction.  This fundamental observation has raised important
questions particularly its relationship to the pathogenesis of arthritis
such as why should chondrocytes express la antigen?  Does la on
chondrocytes have a role in initiating autoimmunity?  Is it possible that
during a pathological state, such as in immune arthritis, la expression on
chondrocytes is up-regulated?  Is la expression on these cells a marker of
cell differentiation?  Does la antigen on chondrocytes have a role in the
morphogenesis of cartilage tissue.  Our investigations have opened a new
field of research investigation in which a thorough comparison of the
immune function of chondrocytes particularly antigen presenting activity
needs to be investigated and compared to the cells such as macrophages.
The above functions include the synthesis of the factor like interleukin-1
by chondrocytes.  A systemic investigation is needed to explore the
cellular interactions mediated by chondrocytes, first during in vitro
immune responses and later in vivo arthritis disease models.  The presence
of la antigen on chondrocytes leads us to believe, the hypothesis, that it
may have a role in the pathogenesis of immune or even nonimmune form of
arthritis.  Chondrocytes are secluded by virtue of being embedded in matrix
from immunoglobulins and lymphocytes but can be liberated by matrix
degrading enzyme such as in immune complex induced inflammation.
Chondrocyte upon interaction with lymphocytes can be perceived as foreign
through the presence of la antigen and immune cells initiate a form of
autoimmune reactivity.  This local reactivi...

## Key facts

- **NIH application ID:** 3159022
- **Project number:** 5R01AR038971-03
- **Recipient organization:** UNIV OF MED/DENT NJ-R W JOHNSON MED SCH
- **Principal Investigator:** MOTI L TIKU
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $115,133
- **Award type:** 5
- **Project period:** 1987-01-01 → 1989-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3159022

## Citation

> US National Institutes of Health, RePORTER application 3159022, IMMUNOBIOLOGY OF CHONDROCYTES (5R01AR038971-03). Retrieved via MORVS 2026-10-24 from https://api.morvs.ai/grant/nih/3159022. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*