Identification of basophils by a mAb directed against pro–major basic protein 1

Plager, Douglas A.; Weiss, Ellen A.; Kephart, Gail M.; Mocharla, Robert; Matsumoto, Ryoji; Checkel, James L.; Schwartz, Lawrence B.; Gleich, Gerald J.; Leiferman, Kristin M.

doi:10.1016/j.jaci.2005.10.023

Cited by 41 publications

(24 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…89 Basophil involvement in anaphylaxis will likely be further elucidated in the future because a monoclonal antibody directed against pro-major basic protein 1 has been identified. 90 The opening of the endothelial barrier through endothelial G q /G 11 -mediated signaling has been identified as a critically important process leading to symptoms of anaphylaxis in many body organ systems. 91 There are few studies of the role of genetic factors in human anaphylaxis.…”

Section: Pathogenesis Triggers Of Anaphylaxismentioning

confidence: 99%

Anaphylaxis

Simons

2010

Journal of Allergy and Clinical Immunology

397

380

View full text Add to dashboard Cite

Anaphylaxis occurs commonly in community settings. The rate of occurrence is increasing, especially in young people. Understanding potential triggers, mechanisms, and patient-specific risk factors for severity and fatality is the key to performing appropriate risk assessment in those who have previously experienced an acute anaphylactic episode. The diagnosis of anaphylaxis is based primarily on clinical criteria and is valid even if the results of laboratory tests, such as serum total tryptase levels, are within normal limits. Positive skin test results or increased serum specific IgE levels to potential triggering allergens confirm sensitization but do not confirm the diagnosis of anaphylaxis because asymptomatic sensitization is common in the general population. Important patient-related risk factors for severity and fatality include age, concomitant diseases, and concurrent medications, as well as other less well-defined factors, such as defects in mediator degradation pathways, fever, acute infection, menses, emotional stress, and disruption of routine. Prevention of anaphylaxis depends primarily on optimal management of patient-related risk factors, strict avoidance of confirmed relevant allergen or other triggers, and, where indicated, immunomodulation (eg, subcutaneous venom immunotherapy to prevent Hymenoptera sting-triggered anaphylaxis, an underused, potentially curative treatment). The benefits and risks of immunomodulation to prevent food-triggered anaphylaxis are still being defined. Epinephrine (adrenaline) is the medication of first choice in the treatment of anaphylaxis. All patients at risk for recurrence in the community should be equipped with 1 or more epinephrine autoinjectors; a written, personalized anaphylaxis emergency action plan; and up-to-date medical identification. Improvements in the design of epinephrine autoinjectors will help to optimize ease of use and safety. Randomized controlled trials of pharmacologic agents, such as antihistamines and glucocorticoids, are needed to strengthen the evidence base for treatment of acute anaphylactic episodes.

show abstract

Section: Pathogenesis Triggers Of Anaphylaxismentioning

confidence: 99%

Anaphylaxis

Simons

2010

Journal of Allergy and Clinical Immunology

397

380

View full text Add to dashboard Cite

show abstract

“…been reported in human disorders such as asthma and atopic dermatitis, [37][38][39][40][41][42] even though the number of infiltrating basophils is usually much smaller than that of other inflammatory cells. The present observations in the mouse model show us that simply because a subpopulation of cells is small does not necessarily mean its biologic role is also small, and therefore it would be worthwhile to reassess the role of basophils in human allergic disorders.…”

Section: Discussionmentioning

confidence: 99%

Basophils are essential initiators of a novel type of chronic allergic inflammation

Obata

Mukai

Tsujimura

et al. 2007

Blood

265

314

View full text Add to dashboard Cite

IntroductionBasophils are the least common leukocytes in the peripheral blood and account for only approximately 0.5% of all leukocytes. Like mast cells, basophils express the high-affinity IgE receptor Fc⑀RI on their cell surface, and they release chemical mediators such as histamine and leukotriene C4 upon stimulation. [1][2][3][4][5] Therefore, basophils have often been neglected or considered minor and possibly redundant "circulating mast cells" and analyzed as a surrogate of the less accessible tissue mast cells. 6 However, basophils and mast cells differ in their natural history. Even though both originate from hematopoietic stem cells in the bone marrow, basophils complete their differentiation in the bone marrow, whereas mast cells do so in the peripheral tissues. 5,7 Basophils circulate in the peripheral blood and do not migrate into the peripheral tissues under physiologic conditions, while mature mast cells reside in the peripheral tissues and do not circulate in the peripheral blood. The lifespan of basophils is several days, much shorter than that of mast cells, and basophils do not proliferate once they mature, unlike mast cells. These differences strongly suggest that basophils and mast cells play distinct roles in vivo.Mast cells and basophils have long been considered primary effector cells in allergic disorders such as anaphylaxis, hay fever, and asthma. 5,7 Recent works demonstrated that mast cells actively participate in the innate immune responses to many pathogens, including bacteria and virus. 8 In addition to such roles as effector cells, recent evidence indicates that mast cells can also play immunoregulatory roles. 9 Mast cells influence the sensitization phase of some acquired immune responses, 10 and contribute to the pathology of autoimmune disorders [11][12][13] and to the expression of peripheral tolerance. 14 Compared with extensive investigation on mast cells and advances in our understanding of mast cell functions, the in vivo roles of basophils are far less studied and defined.A clue to clarifying critical and nonredundant roles of basophils has been provided by the recent finding that basophils readily generate large quantities of T helper 2 (Th2) cytokines such as IL-4 and IL-13 in both humans and mice. [15][16][17][18] These cytokines are the key regulators in conditioning the immune response to the Th2 type. Basophil-derived IL-4 has been shown to drive the differentiation of naive CD4 T cells to Th2 cells in vitro and in vivo. 19,20 Basophils also stimulate B cells to synthesize IgE in vitro in an IL-4-and CD40L-dependent manner. 21,22 We recently identified a novel type of chronic allergic inflammation designated IgEmediated chronic allergic inflammation (IgE-CAI) that requires the presence of basophils, but not mast cells or T cells. 23 A single subcutaneous injection of multivalent antigens elicited not only immediate-and late-phase ear swelling but also delayed-onset ear swelling with massive eosinophil infiltration in mice sensitized with antigen-specific IgE or in mi...

show abstract

“…During allergic inflammation, such as bronchial asthma and atopic dermatitis, basophils infiltrate into peripheral tissues. 16,17 Several lines of evidence have shown that basophils play a major role in allergic reactions and/or immune responses. 18 -21 Basophils initiate IgE-mediated, chronic, cutaneous allergic inflammation (IgE-CAI).…”

mentioning

confidence: 99%

FcεRI, but Not FcγR, Signals Induce Prostaglandin D2 and E2 Production from Basophils

Ugajin

Satoh

Kanamori

et al. 2011

The American Journal of Pathology

View full text Add to dashboard Cite

Prostaglandin (PG) D2 and PGE2 are arachidonic acid metabolites that are generated though an isomerization reaction catalyzed by PG synthases. PGs have been implicated in immunologic reactions in addition to a wide range of physiological functions. It has long been thought that basophils, in contrast to mast cells, do not synthesize PGs, although they do release leukotrienes and platelet-activating factor. Here, we show that basophils function as a source of PGD2 and PGE2. In vitrocultured basophils from mouse bone marrow produced both PGD2 and PGE2 in response to IgE ؉ antigen (Ag), but not to IgG ؉ Ag. Release of PGs was almost completely abrogated in cultured basophils from FcR␥-chain ؊/؊ mice, indicating the involvement of Fc RI. Basophils freshly isolated from bone marrow cells (primary basophils) were also capable of secreting PGD2 and PGE2. Although the amount of PGD2 released from primary basophils was lower than that from mast cells, the capability of primary basophils to generate PGE2 was more potent than that of mast cells. Transcripts and proteins for both hematopoietic-type PGD synthase and PGE synthase were detected in basophils. In addition, human basophils, like mouse basophils, also produced PGD2 through IgE-mediated stimulation. Thus, basophils could be an important source of PGD2/ PGE2 and may contribute to allergic inflammation and immune responses. Prostaglandins, such as PGD2 and PGE2, are cyclooxygenase (COX) metabolites of arachidonic acids. They have a wide range of biological activities, including relaxation and contraction of smooth muscles, and modulation of neuronal activity. 1 PGD2 is principally produced by activated mast cells and, to a lesser extent, by T helper cell 2 (Th2) cells and dendritic cells 2-4 and exerts its effect through D prostanoid 5 and chemoattractant receptor-homologous molecule receptors expressed onTh2 lymphocytes (CRTH2). 6 A number of recent studies have shown that PGD2 is involved in inflammatory reactions. Mast cell-derived PGD2 suppresses IL-12 production by dendritic cells that induce Th2 responses in vivo. 7 PGD2 both activates and induces chemotaxis of Th2 cells, eosinophils, and basophils. 6 A large amount of PGD2 is detected in broncho-alveolar lavage fluid during allergen-induced airway inflammation. 8 Transgenic mice overexpressing human PGD synthase showed exacerbation of ovalbumin (OVA)-induced lung inflammation associated with pronounced eosinophilia and increased Th2 cytokine production. 9 In our previous studies, mice deficient in the CRTH2 gene were characterized by alleviated IgE-mediated cutaneous responses, contact hypersensitivity reactions, 10 and cedar pollen dermatitis. 11 However, PGE2 is produced by a variety of cells, including fibroblasts and macrophages, and exerts its effects via prostaglandin E2 (EP)1, EP2, EP3, and EP4 receptors. 12 PGE2 acts on T cells to enhance production of Th2-type cytokines and to inhibit production of Th1 cytokines in vitro, 13 whereas another study showed that PGE2 facilitates Th1 differentiation via EP...

show abstract

Identification of basophils by a mAb directed against pro–major basic protein 1

Cited by 41 publications

References 44 publications

Anaphylaxis

Anaphylaxis

Basophils are essential initiators of a novel type of chronic allergic inflammation

FcεRI, but Not FcγR, Signals Induce Prostaglandin D2 and E2 Production from Basophils

Contact Info

Product

Resources

About