Armando,
would you agree with this:
[0001] The ability of the mammalian immune system to recognize "self" versus "non-self" antigens is vital to successful host defense against invading microorganisms. "Self" antigens are those which are not detectably different from an animal's own constituents, whereas "non-self" antigens are those which are detectably different from or foreign to the mammal's constituents. A normal mammalian immune system functions to recognize "non-self antigens" and attack and destroy them. An autoimmune disorder such as for example, rheumatoid arthritis, insulin-independent diabetes mellitus, acquired immune deficiency syndrome (AIDS), multiple sclerosis, and the like, results when the immune system identifies "self" antigens as "non-self", thereby initiating an immune response against the mammal's own body components (i.e., organs and/or tissues). This creates damage to the mammal's organs and/or tissues and can result in serious illness or death.
[0002] Predisposition of a mammal to an autoimmune disease is largely genetic; however, exogenous factors such as viruses, bacteria, or chemical agents may also play a role. Autoimmunity can also surface in tissues that are not normally exposed to lymphocytes such as for example, neural tissue. When a tissue not normally exposed to lymphocytes becomes exposed to these cells, the lymphocytes may recognize the surface antigens of these tissues as "non-self" and an immune response may ensue. Autoimmunity may also develop as a result of the introduction into the animal of antigens which are sensitive to the host's self antigens. An antigen which is similar to or cross-reactive with an antigen in an mammal's own tissue may cause lymphocytes to recognize and destroy both "self" and "non-self" antigens.
[0003] It has been suggested that the pathogenesis of autoimmune diseases is associated with a disruption in synthesis of interferons and other cytokines often induced by interferons (Skurkovich et al., Nature 217:551-552, 1974; Skurkovich et al., Annals of Allergy, 35:356, 1975; Skurkovich et al., J. Interferon Res. 12, Suppl. 1:S110, 1992; Skurkovich et al., Med. Hypoth., 41:177-185, 1993; Skurkovich et al., Med. Hypoth., 42:27-35, 1994; Gringeri et al., Cell. Mol. Biol. 41(3):381-387, 1995; Gringeri et al., J. Acquir. Immun. Defic. Syndr., 13:55-67, 1996). Cytokines are substances produced in different cell territories, including immune and nerve cells, which communicate with and affect the action of cells. In particular, interferon (IFN) gamma plays a significant pathogenic role in autoimmune dysfunction. gamma interferon stimulates cells to produce elevated levels of HLA class II antigens (Feldman et al., 1987, "Interferons and Autoimmunity", In: IFN .gamma., p. 75, Academic Press). It is known that gamma interferon participates in the production of tumor necrosis factor (TNF), and it is also known that TNF also plays a role in stimulation of production of autoantibodies. In view of this, therapies to modulate these cytokines have been developed. Clinical success in treating several autoimmune diseases using antibodies to gamma interferon has been reported (Skurkovich et al., U.S. Pat. No. 5,888,511).
[0004] However, while an autoimmune response is considered to be typical in diseases such as multiple sclerosis and rheumatoid arthritis, one area of medicine where treatment of autoimmune or hyperimmune responses has not been fully explored is the area of skin diseases, particularly inflammatory skin diseases or skin diseases with an autoimmune component. Inflammation and autoimmune responses arising from antigens and the reaction of the skin to antigens is typical in skin diseases. Inflammation is the organism's normal reaction to invading foreign antigens.
[0005] Inflammation and autoimmune reactions in the skin are of considerable concern. Skin diseases including psoriasis, dermatitis, allergic conditions such as eczema, skin hypersensitivity reactions (including poison ivy and poison oak), decubitus ulcers, pressure ulcers, diabetic ulcers, epidermolysis bullosa, and milia psoriasis, atopic dermatitis, contact dermatitis, eczematoid dermatitis, seborrheic dermatitis, lichen planus, pemphigus, bullous pemphigoid, epidermolysis bullosa, urticaria, angioedema, vasculitides, erythema, dermal eosinophilia, acne, vitiligo and alopecia areata may also be the result of an inflammatory or autoimmune reaction in the skin.
[0006] Of these and other skin diseases, the most prevalent is acne. Acne, specifically acne vulgaris is a skin disease that is estimated to affect 85-100% of the population at one time in their life. Acne vulgaris is characterized by non-inflammatory follicular papules or comedones and by inflammatory papules, pustules and nodules. Areas of the skin with the most dense concentration of sebaceous follicles, usually the face, the upper chest and the back, are most commonly prone to acne vulgaris. Acne vulgaris is more common in men than in women during adolescence, but is more common in women during adulthood. Acne vulgaris may also occur in newborns, but often resolves when androgen levels begin to rise.
[0007] At least four factors are important in the development of acne lesions; follicular epidermal hyperproliferation and hyperkeratinization, excess sebum, Propionibacterium acnes, and inflammation. Follicular epidermal hyperproliferation and hyperkeratinization may be stimulated by increased levels of androgens and the alteration in the sebum and lipid levels in acne lesions. In addition, the presence of interleukin-1-alpha (IL-1.alpha.) may lead to hyperkeratinization and hyperproliferation of the infudibulum (Zouboulis, 2001, Dermatology 203: 277-279).
[0008] Excess sebum is strongly correlated with the degree and severity of acne lesions. Androgens stimulate sebum production and estrogens inhibit sebum production, and therefore an excess level of androgens or a hyperresponse to androgens may lead to acne lesion formation.
[0009] Propionibacterium acnes is a microaerophilic bacteria present in many acne lesions, but may not be present in the nascent acne lesion. It is widely accepted that the inflammation in acne is due to the immunological reaction to the extracellular products of P. acnes, such as free fatty acids (Zouboulis, 2001, Dermatology 203: 277-279). P. acnes may also bind to the toll-like receptors on monocytes, initiating the production of cytokines such as tumor necrosis factor, IL-12 and IL-8.
Perhaps lessening sebum secretion could be beneficial for androgenic alopecia if excessive sebum is playing a part in inducing an immuno respone at the infidulum.
Armando, I know you think this is due to cutting the hair and not wearing it long.......................but if this little hypothesis of sebum playing a role was "right" and it is an aggravating factor in human beings...................a topical that lessens sebum production, a daily washing of the hair to remove sebum, and perhaps a few minutes of the scalp excercises before one washes the hair to get as much of it as possible to the top of the dermis so it can be removed by washing would probably be a better method of helping than just growing one's hair really long. I have medium length hair (3 inches, maybe a bit more), kinda "Beatlesque" in length. I have no desire to wear hair to my shoulders at my age now.
