An Immunoglobulin (IgG) Inhibitor of Polymorphonuclear Leukocyte Motility in a Patient with Recurrent Infection

Neil Kramer, H. Daniel Perez, Ira M. Goldstein

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

We isolated from the serum of a patient with recurrent skin infections an IgG immunoglobulin that irreversibly inhibits the random motility and chemotactic responsiveness of polymorphonuclear leukocytes. Although the patient's leukocytes behaved like normal cells with respect to adherence, phagocytosis, degranulation, and generation of the superoxide anion, they did not migrate normally toward standard chemotactic stimuli. Normal human polymorphonuclear leukocytes behaved similarly after incubation with the patient's serum. Inhibition of motility was not associated with cytotoxicity. Inhibitory activity could be removed completely from the patient's serum by treatment with either agarose-bound anti-human IgG or Sepharose-bound staphylococcal protein A. Exposure of normal polymorphonuclear leukocytes to as little as 1.25 μg per milliliter (0.00125 g per liter) of the patient's purified IgG caused significant inhibition of random motility and chemotactic responsiveness (P<0.01). Thus, IgG immunoglobulins can inhibit leukocyte motility specifically and irreversibly, and thereby adversely affect host defenses against invading microorganisms. (N Engl J Med. 1980; 303:1253–8.) THE ability of polymorphonuclear leukocytes (PMN's) to migrate in a directed fashion along gradients of chemotactic stimuli appears to be essential for the maintenance of normal host defenses against invading microorganisms.1,2 Indeed, several abnormalities of PMN random motility and chemotactic responsiveness have been identified in patients with increased susceptibility to recurrent bacterial infections.3 4 5 6 7 Although some of these abnormalities have been associated with other defective PMN functions (e.g., adherence, phagocytosis, degranulation, and oxidative metabolism), there is ample evidence that impaired motility alone may be sufficient to affect host defenses adversely. For example, PMN's from some patients with hyperimmunoglobulin E and recurrent.

Original languageEnglish (US)
Pages (from-to)1253-1258
Number of pages6
JournalNew England Journal of Medicine
Volume303
Issue number22
DOIs
StatePublished - Nov 27 1980
Externally publishedYes

Fingerprint

Immunoglobulins
Neutrophils
Immunoglobulin G
Infection
Phagocytosis
Leukocytes
Serum
Staphylococcal Protein A
Superoxides
Sepharose
Maintenance
Skin

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

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title = "An Immunoglobulin (IgG) Inhibitor of Polymorphonuclear Leukocyte Motility in a Patient with Recurrent Infection",
abstract = "We isolated from the serum of a patient with recurrent skin infections an IgG immunoglobulin that irreversibly inhibits the random motility and chemotactic responsiveness of polymorphonuclear leukocytes. Although the patient's leukocytes behaved like normal cells with respect to adherence, phagocytosis, degranulation, and generation of the superoxide anion, they did not migrate normally toward standard chemotactic stimuli. Normal human polymorphonuclear leukocytes behaved similarly after incubation with the patient's serum. Inhibition of motility was not associated with cytotoxicity. Inhibitory activity could be removed completely from the patient's serum by treatment with either agarose-bound anti-human IgG or Sepharose-bound staphylococcal protein A. Exposure of normal polymorphonuclear leukocytes to as little as 1.25 μg per milliliter (0.00125 g per liter) of the patient's purified IgG caused significant inhibition of random motility and chemotactic responsiveness (P<0.01). Thus, IgG immunoglobulins can inhibit leukocyte motility specifically and irreversibly, and thereby adversely affect host defenses against invading microorganisms. (N Engl J Med. 1980; 303:1253–8.) THE ability of polymorphonuclear leukocytes (PMN's) to migrate in a directed fashion along gradients of chemotactic stimuli appears to be essential for the maintenance of normal host defenses against invading microorganisms.1,2 Indeed, several abnormalities of PMN random motility and chemotactic responsiveness have been identified in patients with increased susceptibility to recurrent bacterial infections.3 4 5 6 7 Although some of these abnormalities have been associated with other defective PMN functions (e.g., adherence, phagocytosis, degranulation, and oxidative metabolism), there is ample evidence that impaired motility alone may be sufficient to affect host defenses adversely. For example, PMN's from some patients with hyperimmunoglobulin E and recurrent.",
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An Immunoglobulin (IgG) Inhibitor of Polymorphonuclear Leukocyte Motility in a Patient with Recurrent Infection. / Kramer, Neil; Perez, H. Daniel; Goldstein, Ira M.

In: New England Journal of Medicine, Vol. 303, No. 22, 27.11.1980, p. 1253-1258.

Research output: Contribution to journalArticle

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T1 - An Immunoglobulin (IgG) Inhibitor of Polymorphonuclear Leukocyte Motility in a Patient with Recurrent Infection

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AU - Perez, H. Daniel

AU - Goldstein, Ira M.

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N2 - We isolated from the serum of a patient with recurrent skin infections an IgG immunoglobulin that irreversibly inhibits the random motility and chemotactic responsiveness of polymorphonuclear leukocytes. Although the patient's leukocytes behaved like normal cells with respect to adherence, phagocytosis, degranulation, and generation of the superoxide anion, they did not migrate normally toward standard chemotactic stimuli. Normal human polymorphonuclear leukocytes behaved similarly after incubation with the patient's serum. Inhibition of motility was not associated with cytotoxicity. Inhibitory activity could be removed completely from the patient's serum by treatment with either agarose-bound anti-human IgG or Sepharose-bound staphylococcal protein A. Exposure of normal polymorphonuclear leukocytes to as little as 1.25 μg per milliliter (0.00125 g per liter) of the patient's purified IgG caused significant inhibition of random motility and chemotactic responsiveness (P<0.01). Thus, IgG immunoglobulins can inhibit leukocyte motility specifically and irreversibly, and thereby adversely affect host defenses against invading microorganisms. (N Engl J Med. 1980; 303:1253–8.) THE ability of polymorphonuclear leukocytes (PMN's) to migrate in a directed fashion along gradients of chemotactic stimuli appears to be essential for the maintenance of normal host defenses against invading microorganisms.1,2 Indeed, several abnormalities of PMN random motility and chemotactic responsiveness have been identified in patients with increased susceptibility to recurrent bacterial infections.3 4 5 6 7 Although some of these abnormalities have been associated with other defective PMN functions (e.g., adherence, phagocytosis, degranulation, and oxidative metabolism), there is ample evidence that impaired motility alone may be sufficient to affect host defenses adversely. For example, PMN's from some patients with hyperimmunoglobulin E and recurrent.

AB - We isolated from the serum of a patient with recurrent skin infections an IgG immunoglobulin that irreversibly inhibits the random motility and chemotactic responsiveness of polymorphonuclear leukocytes. Although the patient's leukocytes behaved like normal cells with respect to adherence, phagocytosis, degranulation, and generation of the superoxide anion, they did not migrate normally toward standard chemotactic stimuli. Normal human polymorphonuclear leukocytes behaved similarly after incubation with the patient's serum. Inhibition of motility was not associated with cytotoxicity. Inhibitory activity could be removed completely from the patient's serum by treatment with either agarose-bound anti-human IgG or Sepharose-bound staphylococcal protein A. Exposure of normal polymorphonuclear leukocytes to as little as 1.25 μg per milliliter (0.00125 g per liter) of the patient's purified IgG caused significant inhibition of random motility and chemotactic responsiveness (P<0.01). Thus, IgG immunoglobulins can inhibit leukocyte motility specifically and irreversibly, and thereby adversely affect host defenses against invading microorganisms. (N Engl J Med. 1980; 303:1253–8.) THE ability of polymorphonuclear leukocytes (PMN's) to migrate in a directed fashion along gradients of chemotactic stimuli appears to be essential for the maintenance of normal host defenses against invading microorganisms.1,2 Indeed, several abnormalities of PMN random motility and chemotactic responsiveness have been identified in patients with increased susceptibility to recurrent bacterial infections.3 4 5 6 7 Although some of these abnormalities have been associated with other defective PMN functions (e.g., adherence, phagocytosis, degranulation, and oxidative metabolism), there is ample evidence that impaired motility alone may be sufficient to affect host defenses adversely. For example, PMN's from some patients with hyperimmunoglobulin E and recurrent.

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