instruction:
In this task, you're given a paragraph from the research paper and your task is to generate a suitable title for the research paper based on the given paper. Under 100 words is a good title length.
question:
Many acute infectious pulmonary diseases have incubation periods that are long enough for travelers to have symptoms after returning home to a health-care system that is not familiar with "foreign" infections. Respiratory infections have a relatively limited repertoire of clinical manifestations, so that there is often nothing characteristic enough about a specific infection to make the diagnosis obvious. Thus, the pathway to the diagnosis of infections that are not endemic in a region relies heavily on taking a thorough history of both itinerary and of specific exposures. One important caveat is that on occasion, the history of a recent trip creates an element of "tunnel vision" in the evaluating health-care provider. It is tempting to relate a person's problem to that recent trip; however, when evaluating recent returnees, it is always important to remember that the travel may have nothing to do with the patient's presentation. Recent travel may add diagnostic considerations to the list of possibilities, but an astute clinician must not disregard the possibility that the patient's illness has nothing to do with the recent trip. (CHEST 2008; 134:163-171) 
answer:
Acute Respiratory Infections in a Recently Arrived Traveler to Your Part of the World*


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We live in a hostile environment, surrounded by microbial pathogens and subject to a range of physical and chemical insults. To survive in this environment, vertebrates have evolved complex immune systems. A key element of this defence is the deployment of rapid response elements at the most probable sites of attack, which are the epithelial-cell boundaries between the body and the environment in the skin, gut and lungs. As the body's largest and most exposed interface with the environment, the skin has a central role in host defence. Before the relatively recent discovery of the immunological defences of skin, the cutaneous interface was viewed as a passive barrier between the host and the hostile environment. In the past few decades, however, it has become apparent that the mechanical aspects of epidermal defence are reinforced by a versatile and robust system of immune surveillance 1 (FIG. 1) . The crucial role of immune surveillance in maintaining homeostasis is evident from the marked increase in the frequency and severity of cutaneous malignancies and infections when immune function is limited, for example in patients with genetic and acquired immunodeficiency disorders and in those receiving immunosuppressive therapy after organ transplantation 2,3 . The regulation of skin defence mechanisms is also crucial, as inappropriate or misdirected immune activity is implicated in the pathogenesis of a large variety of acquired inflammatory skin disorders, including psoriasis, atopic and allergic contact dermatitis, lichen planus, alopecia areata and vitiligo 4-10 . The role of immune dysfunction in these conditions is emphasized by their response to immunosuppressive therapeutic interventions [11] [12] [13] [14] . Understanding the mechanisms of immune surveillance in the skin and tissue-specific immune responses also has important implications for the rational design of vaccines. To promote protective immunity, an immunization protocol must elicit not only an antigenspecific immune response, but also an effective memory response that will provide long-lived protection at the most probable sites of invasion. This applies equally to immunization against infectious organisms, which in most cases invade through the skin or the epithelia of the gastrointestinal or respiratory systems, and to the elicitation of immune responses against tumours. As we discuss, the route and means of adjuvant stimulation that is used can affect the effectiveness and utility of specific vaccine strategies. In this review, we discuss these issues in the context of recent advances in our understanding of cutaneous immune mechanisms, highlighting the interaction of The skin, as the primary interface between the body and the environment, provides the first line of defence against a broad array of microbial pathogens and trauma. In addition to its properties as a physical barrier, the skin has many active defence mechanisms. In this review, we discuss the interaction between the innate and adaptive immune systems in the skin as a model for immune function at epithelial-cell interfaces with the environment. How these mechanisms account for the robust nature of cutaneous immune surveillance and how their dysregulation drives the pathogenesis of inflammatory skin disorders and skin-based tumours are the subjects of this review.
answer:
IMMUNE SURVEILLANCE IN THE SKIN: MECHANISMS AND CLINICAL CONSEQUENCES


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Recent studies in mice have demonstrated that the protein tyrosine phosphatase SHP-1 is a crucial negative regulator of pro-inflammatory cytokine signaling, TLR signaling, and inflammatory gene expression. Furthermore, mice genetically lacking SHP-1 (me/me) display a profound susceptibility to inflammatory CNS demyelination relative to wild type mice. In particular, SHP-1 deficiency may act predominantly in inflammatory macrophages to increase CNS demyelination as SHP-1-deficient macrophages display co-expression of inflammatory effector molecules and increased demyelinating activity in me/me mice. Recently, we reported that PBMCs of multiple sclerosis (MS) patients have a deficiency in SHP-1 expression relative to normal control subjects indicating that SHP-1 deficiency may play a similar role in MS as to that seen in mice. Therefore, it became essential to examine the specific expression and function of SHP-1 in macrophages from MS patients. Herein, we document that macrophages of MS patients have deficient SHP-1 protein and mRNA expression relative to those of normal control subjects. To examine functional consequences of the lower SHP-1, the activation of STAT6, STAT1, and NF-κB was quantified and macrophages of MS patients showed increased activation of these transcription factors. In accordance with this observation, several STAT6-, STAT1-, and NF-κB-responsive genes that mediate inflammatory demyelination were increased in macrophages of MS patients following cytokine and TLR agonist stimulation. Supporting a direct role of SHP-1 deficiency in altered macrophage function, experimental depletion of SHP-1 in normal subject macrophages resulted in an increased STAT/NF-κB activation and increased inflammatory gene expression to levels seen in macrophages of MS patients. In conclusion, macrophages of MS patients display a deficiency of SHP-1 expression, heightened activation of STAT6, STAT1, and NF-κB and a corresponding inflammatory profile that may be important in controlling macrophage-mediated demyelination in MS. Patients and normal subjects donated 50 ml of blood collected in heparinazed tubes. Blood was diluted 1:1 with Hank's balanced salt solution (HBSS) and overlaid onto lymphocyte Christophi et al.
answer:

Macrophages of multiple sclerosis patients display deficient SHP-1 expression and enhanced inflammatory phenotype HHS Public Access