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Monocytotoxic antilodies in SLE patients.

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Table 2. The Development of the Humoral and Cell-Mediated Immune
Response to EL, Cells in Lewis Rats Injected Intraperironeally with
a Suspension of 5 X 10’ EL, Cells in 0.4 ml of I ) Saline, 2 ) Complete
Freund’s Adjuvant, and 3) a Solution of Alkyldiamine (CP20961) in
Mineral Oil (50 mglml). Seven Animals Were Used for Each Group
EL, cells + saline
EL, cells + M butyricum
+ mineral oil
EL, cells + CP-20961
+ mineral oil
* Means
Immune Response
(% “Cr release)
Mean f SD
10.7 f 0.6
43.6 & 1.2
53.0 & 0.2
of two determinations with pooled sera.
that suggested that the induction of the disease does not
involve an immune response to alkyldiamine. The alkyldiamine was found to be a potent adjuvant. The development of the cell-mediated and humoral immune
response to EL, cells in rats (measured by complementindependent spleen lymphocyte lysis of 51Crlabeled EL,
cells and complement dependent antibody lysis of “Cr
labeled EL, cells respectively as previously described
( I ) was greatly enhanced by coadministration of a solution of CP-20961 in mineral oil (Table 2). These findings
suggest that the irnmunogen responsible for the development of adjuvant arthritis is endogenous, for example, a
constituent of host tissue, a viral protein, or some complex of the two.
Certain aqueous formulations of CP-20961 have
been shown to induce production of interferon and to
have antiviral activity (10,ll). The arthritogenic activity
is probably not associated with these effects since administration of oily preparations of other interferon inducers, that is, poly 1:C or tilorone failed to induce
adjuvant arthritis (Table 1 ).
UCLA School of Medicine
1000 Veteran Avenue
Los Angeles, California 90024
I . Chang YH: Adjuvant polyarthritis. 11. Suppression by
tilorone. J Phar Exp Ther (in press) 1977
2. Chang YH, Hoffman WW: Adjuvant polyarthritis. I l l .
Suppression by interferon. Arthritis Rheum 207, 1977
3. Pearson CM: Development of arthritis, periarthritis and
periostitis in rats given adjuvants. Proc SOCExp Biol Med
91:95, 1956
4. Paronetto F: Studies on experimental arthritis induced by
Cornebacterium rubrum. I. Localization of the arthritogenic factor in the cell walls. Arthritis Rheum 15:36, 1972
5. Cromarite WJ, Craddock JG, Schwab JH: Production of
chronic arthritis in rats with group A streptococcal cellular components. Fed Proc 27:477, 1968
6. Kohashi 0, Pearson CM, Watanabe Y, Kotani S, Koga,
T: Structural requirements for arthritogenicity of peptidoglycans from staphylococcus awes and lactobacillus
plantarium and analogous synthetic compounds. J Immuno1 116:1635, 1976
7. Whitehouse MW, Orr KJ, Beck FWJ, Pearson CM:
Freund’s adjuvants: relationship of arthritogenicity and
adjuvanticity in rats to vehicle composition. lmmunol
27:31 I . 1974
8. Glenn, EM, Gray J: Adjuvant-induced polyarthritis in
rats: biologic and histologic background. Am J Vet Res
26:l 180, 1965
9. Pearson C M , Wood FD, and Tanaka A: Antigenicity of
mycobacterial subfractions and adjuvant-induced arthritis. Program of Annual Meeting of American Rheumatism Association, abstract 57, 1968
10. Hoffman WW, Korst JJ, Niblack JF, Cronin TH: N,NDioctadecyl-N’. N’-bis (2-hydroxyethyl) propanediamine.
Antiviral activity and interferon stimulation in mice. Antimicrobial. Agents Chemother 3:498. 1973
I I . Douglas RG, Betts RF, Simons RL. Hoga PW. Roth FK:
Evaluation of a topical interferon inducer in experimental
influenza infection in volunteers. Antimicrobiol Agents
Chemother 8:684. 1975
Monocytotoxic Antibodies in SLE Patients
To the Editor:
I read with interest the article of Dr. Arend, et
20: 1049, 1977, regarding monocytotoxic antibodies in patients with systemic
lupus erythematosus. Although the authors referred to
o u r paper describing monocytotoxic activity of cold agglutinins (ref 29), they missed our publication entitled
“Cytotoxic Antibodies Against Lymphocytes, Granulocytes and Monocytes in Collagen Diseases,” which
was reported in the form of an abstract (Clin Research
24:674, 1976).
We found that quite a substantial proportion of
;era from patients with systemic lupus erythematosus,
rheumatoid arthritis, Felty’s syndrome and less with
other rheumatic diseases, had heterogeneous population
of autoantibodies cytotoxic to lymphocytes, granulocytes, and monocytes. Some of these antibodies were
reactive in the cold, whereas others were capable of
killing cells at 37°C. In the majority of instances, these
antibodies required nonhuman complement to be activated; however, in a few instances (especially in the case
of monocytotoxins) cytotoxic activity was observed in
the absence of rabbit serum. At the present time we have
eluted these cytotoxic antibodies from various cells. We
found that some eluates were capable of killing more
than one type of cell thus implying an existence of
common antigenic determinants. I would like to stress
that studies of monocytotoxic antibodies are complicated by the fact that the monocytes in part are lysed
during the monocytotoxicity assay, thus escaping trypan-blue staining.
M.D., F.R.C.P.(C)., F.A.C.P.
Professor of Medicine
Immunoglobulin Diagnostic & Research Centre
University of Toronto
Toronto, Canada
Declassification of Arteritis
To the Editor:
I was interested in the comments by Dr. Sergent
in the June issue case report of a patient with systemic
vasculitis. Since the original classification of arteritis by
Zeek et al. ( I ) , it has become apparent that many patients do not satisfy the criteria for any one of the types
of described vasculitides. The physician is often left with
a poorly defined illness to which he has to ascribe a
diagnosis that is neither complete nor satisfactory. In a
recent article by Alarc6n-Segovia (2), the author proposes a classification by delineating the potential etiologies of the vasculitic syndrome along with their characteristic clinical pictures.
In trying to deal with the large number of variables that one might encounter with a vasculitic syndrome, such as the etiologic associations as defined by
Dr. Sergent (cryoglobulinemia, hepatitis-associated antigen, or drugs) and the different clinical presentations
such as neuropathy, skin ulcers, or renal disease, I
would propose a “declassification” of arteritis that is
based on the New York Heart Association’s criteria for
cardiac disease. For example, a patient such as the one
described in the case report would have a diagnosis of
vasculitis, etiology unknown; pathoanatomical diagnosis-necrotizing vasculitis involving the small and me-
dium size arteries; physiologic diagnosis-mononeuropathy multiplex.
This description of disease would alleviate the
confusion arising out of whether the patient has polyarteritis, the vasculitis associated with rheumatoid arthritis, hypersensitivity angiitis or whatever. Additionally, a diagnosis could be made based on the available
information only.
Appalachian Arthritis Foundation &
Section of Rheumatology
Department of Medicine
University of Tennessee
Clinical Education Center
Chattanooga, Tennessee
I . Zeek PM: Periarteritis nodosa and other forms of necrotizing arteritis. N Engl J Med 248:764, 1953
2. Alarc6n-Segovia D: The necrotizing vasculitides. Med Clin
N Am 61:241-259, 1977
Clinical Drug Efficacy and in Vitro
Inhibition of Lymphocyte Responses in
Rheumatoid Arthritis
To the Editor:
Mechanisms of antiinflammatory effects of
drugs are not known (1). Among other actions
many antirheumatic drugs affected in vitro responsiveness of normal human peripheral blood lymphocytes (PBL) (2,3). Also, responses of patients with
rheumatoid arthritis (RA) to individual drugs are
often unpredictable, We therefore examined possible
relationships between in vitro drug effects and subsequent clinical responses of patients to those drugs
during clinical trials.
Seventeen patients with RA were studied. Patients’ PBL, obtained after drug therapy was discontinued for more than 48 hours, were placed into
short-term cultures with or without mitogens and
with or without drugs, as described (2). We determined inhibition of stimulated PBL responses by
aspirin (ASA), 80 pg/ml; indomethacin (IND), 350
pg/ml; naproxen (NAP), 300 pg/ml; and sodium
meclofenamate (MFA), 175 pg/ml-concentrations
approximating 50% inhibitory dosages for normal
PBL (2). Degree of i n vitro inhibition was related
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