Fondaparinux as an alternative therapy in heparin-induced delayed-type hypersensitivity skin lesions

Delayed skin reactions were produced in rabbits with relatively low serum antibody titers by a single injection of a small amount of horseradish peroxidase (HRP) or of rat anti-HRP γ-globulin in complete Freund's adjuvant into the footpads. One to 2 days after skin testing, the reaction for the specific antibody was observed in the delayed skin lesions at the following locations: on the surface of lymphocytes and monocytes (macrophages); in the perinuclear region of small and medium sized lymphocytes; in blast cells; and in cytoplasmic granules of basophil leukocytes. The possible relationship of these antibody locations to delayed type or basophil cutaneous hypersensitivity was discussed. In mixed Arthus-type-delayed type hypersensitivity skin reactions to HRP in animals with high serum antibody titers, a different location of the antibody was observed. In confirmation of earlier data, the reaction occurred in cytoplasmic granules of macrophages and polymorphonuclear leukocytes and in association with collagen fibers, and antigen-antibody complexes accumulated especially in the walls and areas surrounding blood vessels. These localizations of the antibody were considered to be characteristic for Arthus-type hypersensitivity. When rabbits were double immunized against HRP and egg albumin, the reaction for (cytophilic) antibody to HRP on the surface of monocytes, lymphocytes and granulocytes in the upper dermis was as strong in the skin lesion elicited by egg albumin as in that elicited in the same animal by HRP. Lymphocytes with perinuclear antibody appeared in mixed Arthus-type-delayed type hypersensitivity skin reactions to HRP 1-2 days after skin testing but many plasma cells were seen only after 4-5 days in most cases. Observations are also reported on: the persistence of the antigens (HRP and rat anti-HRP γ-globulin) in the skin lesions; the acid phosphatase reaction in cells infiltrating the skin lesions; and cell contact, especially between lymphocytes and macrophages.

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Delayed‐Type Hypersensitivity Skin Testing using Third Variable Loop Peptides Identifies T Lymphocyte Epitopes in Human Immunodeficiency Virus‐Infected Persons

The Journal of Infectious Diseases ◽

10.1086/516517 ◽

1997 ◽

Vol 176 (4) ◽

pp. 1085-1089 ◽

Cited By ~ 11

Author(s):

Karl V. Sitz ◽

Lawrence D. Loomis‐Price ◽

Silvia Ratto‐Kim ◽

Julie R. Kenner ◽

Purnima Sau ◽

...

Keyword(s):

Human Immunodeficiency Virus ◽

T Lymphocyte ◽

Skin Testing ◽

Delayed Type Hypersensitivity ◽

Variable Loop ◽

Immunodeficiency Virus ◽

Hypersensitivity Skin

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Effects of confinement (110 and 240 days) on neuroendocrine stress response and changes of immune cells in men

Journal of Applied Physiology ◽

10.1152/japplphysiol.00732.2001 ◽

2002 ◽

Vol 92 (4) ◽

pp. 1619-1627 ◽

Cited By ~ 22

Author(s):

A. Choukèr ◽

L. Smith ◽

F. Christ ◽

I. Larina ◽

I. Nichiporuk ◽

...

Keyword(s):

Stress Test ◽

Suppressor Cells ◽

Delayed Type Hypersensitivity ◽

Immunological Parameters ◽

Enhanced Expression ◽

Hypersensitivity Skin ◽

Male Subjects ◽

A Current ◽

T Suppressor Cells

The aim of the study was to evaluate the effects of long-term confinement on stress-permissive neuroendocrine and immune responses in humans. Two groups of four male subjects were confined 240 days ( group 240) or 110 days ( group 110) in two space modules of 100 or 200 m3, respectively. During confinement, none of the volunteers developed psychic stress as could be examined and verified by a current stress test. However, in g roup 240 but not in group 110, the diurnal rhythm of cortisol secretion was slightly depressed and the urine excretion of norepinephrine significantly increased. The innate part of the immune system became activated as seen by a rise in the number of circulating granulocytes and the enhanced expression of β2-integrins. In contrast, the ratio of T-helper to T-suppressor cells decreased. All these effects, observed during confinement, were even more pronounced in both groups when values of endocrinological and immunological parameters were compared between before and 1 wk after the end of the confinement period. Hence, return to normal life exerts pronounced effects to a much higher degree, irrespective of how long or under which conditions individuals were confined. Because the delayed-type hypersensitivity skin reaction against recall antigens remained unaffected, it is to be presumed that confinement appears to induce distinct sympathoadrenergic activation and immunological changes but no clinically relevant immunosuppression.

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Pathophysiology of Skin Resident Memory T Cells

Frontiers in Immunology ◽

10.3389/fimmu.2020.618897 ◽

2021 ◽

Vol 11 ◽

Author(s):

Yoshiki Tokura ◽

Pawit Phadungsaksawasdi ◽

Kazuo Kurihara ◽

Toshiharu Fujiyama ◽

Tetsuya Honda

Keyword(s):

Drug Eruption ◽

Transforming Growth Factor ◽

Skin Lesions ◽

Microbial Pathogens ◽

Delayed Type Hypersensitivity ◽

Effector Memory ◽

Lymphoid Tissues ◽

Fixed Drug Eruption ◽

Surveillance Network ◽

Fixed Drug

Tissue resident memory T (TRM) cells reside in peripheral, non-lymphoid tissues such as the skin, where they act as alarm-sensor cells or cytotoxic cells. Physiologically, skin TRM cells persist for a long term and can be reactivated upon reinfection with the same antigen, thus serving as peripheral sentinels in the immune surveillance network. CD8+CD69+CD103+ TRM cells are the well-characterized subtype that develops in the epidermis. The local mediators such as interleukin (IL)-15 and transforming growth factor (TGF)-β are required for the formation of long-lived TRM cell population in skin. Skin TRM cells engage virus-infected cells, proliferate in situ in response to local antigens and do not migrate out of the epidermis. Secondary TRM cell populations are derived from pre-existing TRM cells and newly recruited TRM precursors from the circulation. In addition to microbial pathogens, topical application of chemical allergen to skin causes delayed-type hypersensitivity and amplifies the number of antigen-specific CD8+ TRM cells at challenged site. Skin TRM cells are also involved in the pathological conditions, including vitiligo, psoriasis, fixed drug eruption and cutaneous T-cell lymphoma (CTCL). The functions of these TRM cells seem to be different, depending on each pathology. Psoriasis plaques are seen in a recurrent manner especially at the originally affected sites. Upon stimulation of the skin of psoriasis patients, the CD8+CD103+CD49a- TRM cells in the epidermis seem to be reactivated and initiate IL-17A production. Meanwhile, autoreactive CD8+CD103+CD49a+ TRM cells secreting interferon-γ are present in lesional vitiligo skin. Fixed drug eruption is another disease where skin TRM cells evoke its characteristic clinical appearance upon administration of a causative drug. Intraepidermal CD8+ TRM cells with an effector-memory phenotype resident in the skin lesions of fixed drug eruption play a major contributing role in the development of localized tissue damage. CTCL develops primarily in the skin by a clonal expansion of a transformed TRM cells. CD8+ CTCL with the pagetoid epidermotropic histology is considered to originate from epidermal CD8+ TRM cells. This review will discuss the current understanding of skin TRM biology and their contribution to skin homeostasis and diseases.

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Leukopheresis therapy of leukemic reticuloendotheliosis (hairy cell leukemia)

Blood ◽

10.1182/blood.v54.3.747.747 ◽

1979 ◽

Vol 54 (3) ◽

pp. 747-749 ◽

Cited By ~ 22

Author(s):

JW Fay ◽

JO Moore ◽

GL Logue ◽

AT Huang

Keyword(s):

Lymph Node ◽

Lymph Nodes ◽

Hairy Cell Leukemia ◽

Alternative Therapy ◽

Leukemia Cell ◽

Skin Lesions ◽

Leukemia Cells ◽

Hairy Cell ◽

Cell Leukemia ◽

Cell Counts

Abstract Intensive leukopheresis has been valuable in the short-term palliation of chronic lymphocytic and granulocytic leukemias. A 47-yr-old man with refractory leukemic reticuloendotheliosis (hairy cell leukemia) manifested by anemia, thrombocytopenia, elevated peripheral leukemia cell counts, generalized lymph node enlargement, and leukemic infiltrative skin disease was treated with serial leukopheresis. Removal of approximately 7 X 10(11) peripheral leukemia cells resulted in marked clinical and hematologic improvement with resolution of enlarged lymph nodes and clearing of skin infiltrates. At the time of this reporting, more than 400 wk since the last leukopheresis, the patient continues to do well. The improvement in all blood counts, reduction in lymph node size, and clearing of skin lesions paralleled the reduction of peripheral leukemia cell load by leukopheresis, suggesting mobilization of leukemia cells from marrow, lymph nodes, and skin. Removal of large numbers of leukemia cells in hairy cell leukemia has the potential of achieving sustained clinical improvement and may be a useful alternative therapy for these patients.

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